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TOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY January 1988

Traumatic occupational occlusive arterial disease of the hands

I ALSO: A CASE OF metastatic a community medicine

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A COMMITMENT TO SERVE THE LOUISIANA PHYSICIAN

EDITOR

CONWAY S. MAGEE, MD

CHIEF EXECUTIVE OFFICER
DAVE TARVER

GENERAL MANAGER

RENE ABADIE
MANAGING EDHOR

BONNIE L. BLUNDELL
ADVERTISING SALES

SISSY SULLIVAN HANSEN

JOURNAL COMMITTEE

CONWAY S. MAGEE, MD
Chairman

A.G. KLEINSCHMIDT, JR, MD
PAUL F. LARSON, MD
W. CHARLES MILLER, MD
EMILE K. VENTRE, JR, MD
JAMES W. VILDIBILL, JR, MD
Ex officio

EDITORIAL BOARD

KENNETH B. FARRIS, MD
RODNEY C. JUNG, MD
CONWAY S. MAGEE, MD
W. CHARLES MILLER, MD
ELI SORROW, MD
CLAY A. WAGGENSPACK, JR, MD
WINSTON H. WEESE, MD
PATRICK W. PEAVY, MD

Established 1844. Owned and edited by The
; Journal of the Louisiana State Medical Society, Inc.,
1700 Josephine Street, New Orleans, LA 70113.

Subscription price is $12 per year in advance,
postage paid for the United States; $15 per
year for all foreign countries belonging to the
Postal Union; $1.50 per single issue.

Advertising: Contact Sissy Sullivan Hansen,
1700 Josephine Street, New Orleans, LA 70113;

(504) 561-1033, (800) 462-9508.

Postmaster: Send address changes to 1700
Josephine Street, New Orleans, LA 70113.

The JOURNAL (ISSN 0024-6921) is published
monthly at 1700 Josephine Street, New
Orleans, LA 70113. Second-class postage paid
at New Orleans and additional mailing offices.

Articles and advertisements published in the
JOURNAL are for the interests of its readers and
do not represent the official position or
endorsement of The Journal of the Louisiana State
Medical Society, Inc. or the Louisiana State
Medical Society. The JOURNAL resers'es the
right to make the final decision on all content
and advertisements.

JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY 1988

VOLUME 140 / NUMBER 1 / JANUARY

ARTICLES

Official Call for the 1988
House of Delegates

Terry R. Jones, MD
John D. Fmsha, MD
Jon V. Schellack, MD

Traumatic occupational
occlusive arterial disease
of the hands

David J. Holcombe, MD

A case of metastatic
carcinoma in association
with Paget's disease
of bone

Irwin Cohen, MD

A community medicine
program in Jamaica for
fourth year medical
students

DEPARTMENTS

Information for Authors

New Members

ECG of the Month

Otolaryngology/Head &

Neck Surgery Report

Calendar

Auxiliary Report

Classified Advertising

Books Received

Cover illustration by Eugene New, New Orleans.

INFORMATION FOR AUTHORS

The JOURNAL of the Louisiana State Medical Society is intended to
provide practical scientific information of interest to a broad spectrum
of physician members of the LSMS and to meet the need of each physi-
cian to maintain a general awareness of progress and change in clinical
medicine. The content is designed to aid the practicing physician in
giving comprehensive care and in recognizing the need for special-
ized treatment.

The JOURNAL welcomes material for publication if submitted in ac-
cordance with the following guidelines. Address all correspondence
to the Editor, Journal of the Louisiana State Medical Society, 1700
Josephine Street, New Orleans, LA 701 1 3. Contact the managing editor
with any questions concerning these guidelines or for a checklist to
assist in manuscript preparation.

MANUSCRIPTS should be of an appropriate length due to the policy
of the JOURNAL to feature concise but complete articles. (Some sub-
jects may necessitate exception to this policy and will be reviewed
and published at the Editor's discretion.) The language and vocabulary
of the manuscript should be understandable and not beyond the com-
prehension of the general readership of the journal. The journal
attempts to avoid the use of medical jargon and abbreviations. All ab-
breviations, especially of laboratory and diagnostic procedures, must
be identified in the text. Manuscripts must be typed, double-spaced
with adequate margins. (This applies to all manuscript elements in-
cluding text, references, legends, footnotes, etc.) The original and one
duplicate should be submitted. An accompanying cover letter should
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and telephone number. Manuscripts are received with the explicit
understanding that they have not been previously published and are
not under consideration by any other publication. Manuscripts are sub-
ject to editorial revisions as deemed necessary by the editors and to
such modifications as to bring them into conformity with journal
style. Statements made or opinions expressed by any contributor in
any article or feature published in the journal are the sole respon-
sibility of the author.

REVIEWING PROCESS. Each manuscript is reviewed by the Editor
and by a member(s) of the Editorial Board or the Panel of Consultants
from whom knowledgeable opinions are sought. The acceptability of
a manuscript is determined by such factors as the quality of the
manuscript, perceived interest to journal readers, usefulness or im-
portance to physicians, and the current backlog of accepted
manuscripts. Authors are notified upon receipt of the manuscript. When
acceptability is determined, authors will then be requested to sign a
manuscript consent form transferring copyright privileges to the jour-
nal. Accepted manuscripts become the property of the journal and
may not be published elsewhere, in part or in whole, without permis-
sion from the journal. Abstracts may be reproduced without specific
permission, provided acknowledgement of the source is made.

TITLE PAGE should carry [1] the title of the manuscript, which should
be concise but informative; [2] full name of each author, with highest
academic degree(s), listed in descending order of magnitude of con-
tribution (only the names of those who have contributed materially
to the preparation of the manuscript should be included); [3] a one-
to two-sentence biographical description for each author which should
include specialty, practice location, academic appointments, primary
hospital affiliation, or other credits (a picture, black-and-white head
shot, of each author may also be sent if available); [4] name and ad-
dress of author to whom requests for reprints should be addressed,
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ABSTRACT should be on the second page and consist of no more than
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[3] the material studied; [4] the results obtained. Emphasize new and
important aspects of the study or observations.

KEY WORDS should follow the abstract and be identified as such.
Provide three to five key words or short phrases that will assist index-
ers in cross-indexing your article. Use terms from the Medical Sub-
ject Heading list from Index Medicus when possible.

SUBHEADS are strongly encouraged. They should provide guidance
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text. The format is flexible but subheads ordinarily include: Methods
and Materials, Case Reports, Symptoms, Examination, Treatment and
Technique, Results, Discussion, and Summary.

REFERENCES must be double-spaced on a separate sheet of paper and
limited to a reasonable number. They will be critically examined at
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JOURNALS

[1] Author(s): Use the surname followed by initials without punctua-
tion. The names of all authors should be given unless there are more
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tion, underscored, and abbreviated according to Index Medicus. [4]
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Example: Bora LI, Dannem FJ, Stanford W, et al: A guideline for blood

use during surgery. Am j Clin Pathol 1 979;71 :680-692.

BOOKS

[1] Author(s): Use the surname followed by initials without punctua-
tion. The names of all authors should be given unless there are more
than three, in which case the names of the first three authors are used
followed by "et al." [2] Title, Capitalize the first and last word and
each word that is not an article, preposition, or conjunction of less
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publication, [6] Publisher, [7] Year, [8] Inclusive page numbers. Do
not omit digits.

Example: DeCole EL, Spann E, Flurst RA Jr, et al: Bedside Examina-

tion in Cardiovascular Medicine, ed 2, Smith JT (ed). New
York, McGraw Hill Co, 1986, 23-37.

ILLUSTRATIONS should be submitted in duplicate in an envelope
(paper clips should not be used on illustrations since the indentation
they make may show on reproduction). Legends should be typed on
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specific written consent has been obtained, in which case a copy of
the authorization should accompany the manuscript. Omit illustra-
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TABLES should be self-explanatory and should supplement, not
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numbered, and have a brief descriptive title.

ACKNOWLEDGMENTS are the author's prerogative; however,
acknowledgment of technicians and other remunerated personnel for
carrying out routine operations, or of resident physicians who merely
care for patients as part of their hospital duties is discouraged. More
acceptable acknowledgments include those of intellectual or profes-
sional participation.

GALLEY PROOFS will be mailed to the principal author for correc-
tions. Reprint orders forms will accompany galley proofs.

OFFICIAL

CALL

FOR THE 1988 HOUSE OF DELEGATES □ MARCH 11-13, 1988

IN ACCORDANCE WITH the constitution and bylaws of the Louisiana State Medical Society, the House of Delegates is being
called into annual session at 9 am, Friday, March 11, 1988 at the Le Centre Civique in Lake Charles, Louisiana. The House will
consider such business as presented and required of its annual session. The House will be called to order in the usual manner
and remain in session until its duties are complete.

The delegation representation of the component societies in the House for the 1988 Annual Meeting is as follows:

Acadia

East Baton Rouge

Natchitoches

St Mary

Allen

East & West Feliciana 1

North Central

St Tammany

Ascension

Evangeline

Orleans

Shreveport

Assumption

Franklin

Ouachita

Tangipahoa

Avoyelles

Iberia

Pointe Coupee

Terrebonne

Beauregard

Iberville

Rapides

Tri-Parish

Bossier

Jefferson

River Parishes

Vermillion

Calcasieu

Jefferson Davis

Sabine

Vernon

Catahoula-Concordia

Lafayette

St Bernard

Washington

Claiborne

Lafourche

St Landry

Webster

DeSoto

Morehouse

St Martin

The current general officers, delegates to the AMA, past presidents, past speakers of the House, journal editor, emeritus of-
ficers, district societies and one representative from each medical school are also members of the House of Delegates. The Medical
Student Section is entitled to three delegates and three alternate delegates. The Resident Physician Section is entitled to one delegate
and one alternate.

Component societies

242

District societies

Medical schools

Delegates and alternate delegates to the AMA

Medical Student Section

General officers, past presidents, past speakers of the House,

Resident Physician Section

JOURNAL editor and emeritus officers

Total Delegates

301

REGISTRATION facilities will be maintained for delegates, alternate delegates, officers, executives of the component medical
societies and invited guests. Registration hours will be as follows:

Lake Charles Hilton Le Centre Civique

Thursday, March 10 1 - 5 pm Friday, March 11 8 am - 5 pm

Saturday, March 12 8 am - 5 pm

Sunday, March 13 8 am - noon

JOURNAL VOL 140 JANUARY 3

To help him rebuild his life, you have
many alternatives but only one choice
for comprehensive rehab services.

Many hospitals offer rehab
services, but only the Rehabilitation
Institute of New Orleans can offer
your patient the comprehensive
range of services he needs to fully
explore his capabilities and realize
his potential.

As the largest full-service acute
care rehabilitation hospital in the
Gulf Coast region, F. Edward Hebert
is the primary referral center for
Louisiana and neighboring states.

Our diagnosis-related treatment
teams are separate and complete for
each disability category: spinal cord
injury, brain trauma, stroke, limb
loss, bums, arthritis, neuromuscular
disorders, multiple trauma, and
related disorders. These teams of
specialists provide tightly focused
inpatient and outpatient care to

achieve the best possible results in
the briefest possible time.

At the Rehabilitation Institute
of New Orleans, we rebuild lives.

Rehabilitation Institute
Of New Orleans

We ReBuild lives

F. EDWARD HEBERT HOSPITAL
One Sanctuary Drive, New Orieans, LA 70114, (504) 363-22(X)
METAIRIE OUTPATIENT SERVICES
3001 Division Street ^^200, Metairie, LA 70002, (504) 454-7276

^1 Subsidiaries of Rehab Hospital Services Corporation

4 JOURNAL VOL 140 JANUARY

NEW MEMBERS

Applications for membership have been re-
ceived from the following physicians by the
respective parish medical societies as of Oc-
tober 7, 1987. The Louisiana State Medical
Society is pleased to welcome:

■ Lafayette

Richard L. Fremaux, MD

PO Box 39700, Lafayette 70503

1969, LSU School of Medicine, New Orleans

diagnostic radiology

Arlene C. Richard, M.D,

606 Haifleigh, Franklin 70538

1983, Howard University College of Medi-
cine, Washington, DC

family practice

■ Orleans

Malcolm E. Andry Jr, MD

3439 Prytania, New Orleans 70115
1982, Tulane University School of Medicine
internal medicine

Charles K. Angelo Jr, MD

1202 Monroe St, Gretna 70053
1985, LSU School of Medicine, New Orleans
-general practice

Joanell M. Darnell, MD

1328 Ahne St, New Orleans 70115
1980, LSU School of Medicine, New Orleans
obstetrics/ gynecology

George D. MacEwen, MD

200 Henry Clay Ave, New Orleans 70118
1953, Queens University Faculty of Medi-
cine, Ontario, Canada
orthopedic surgery

William S. Riggins Jr, MD

4700 General Meyer #208, New Orleans
70130

1984, LSU School of Medicine, Shreveport
family practice

Jean Ann Tolmas, MD

2017 Metairie Rd, Metairie 70005

1980 Tulane University School of Medicine

pediatrics

■ Ouachita

Brian W. Alexander, MD

2001 Royal Ave, Monroe 71201
1984, University of Arkansas School of
Medicine
anesthesiology

J, Michael Barraza, MD

3315 Deborah Dr, Monroe 71201

1982, Tulane University School of Medicine

diagnostic radiology

Francis Capalongan, MD

1006 Winnsboro Rd, Monroe 71202
1975, Faculty of Medicine and Surgery Uni-
versity of Santo Tomas, Manila, Philip-
pines
pathology

Dan B. Davidson, MD

3421 Medical Park Dr, Monroe 71211
1975, University of Mississippi School of
Medicine
diagnostic radiology

Noli C. Guinigundo, MD

1300 North Seventh St, West Monroe 71291
1962, Institute of Medicine Far Eastern Uni-
versity, Manila, Philippines
family practice

Robert D. Halsell, MD

2204 Justice St, Monroe 71201

1982, LSU School of Medicine, Shreveport

radiology

William J. Liles Jr, MD

PO Box 8357, Monroe 71211

1979, LSU School of Medicine, Shreveport

pathology

Scott K. McClelland, MD

3510 Medical Park Dr, Monroe 71203
1982, LSU School of Medicine, Shreveport
orthopedic surgery

Owen M. Meyers, MD
714 St John, Monroe 71201
1984, University of Mississippi School of
Medicine
family practice

James T. Rittelmeyer, MD

3510 Medical Park Dr, Monroe 71203
1978, Georgetown University School of
Medicine
cardiology

Joaquin P. Rosales, MD

104 Contempo, West Monroe 71291

1984, LSU School of Medicine, New Orleans

pediatrics

Michael J. Sampognaro, MD

2810 Armand, Monroe 71201

1984, LSU School of Medicine, New Orleans

internal medicine

Richard V. Vines II, MD

312 Grammont #301, Monroe 71201

1984, LSU School of Medicine, Shreveport
internal medicine

■ Intern/ Resident Members

ORLEANS

Stanley M. Bienasz, MD

808 Tullulah, River Ridge 70123

1985, Tulane University School of Medicine
anesthesiology

Adrian B. Blotner, MD

1516 Jefferson Hwy, New Orleans 70121
1984, LSU School of Medicine, New Orleans
psychiatry

Luis G. Uribe, MD

1213 Colony Rd, Metairie 70003
1980, Facultad de Medicina de la Univer-
sidad del Valle, Colombia
internal medicine

ERRATUM

On page 3 of the November 1987 issue
of the JOURNAL, it was stated that
Gail C. Brady, MD was a new
member specializing in internal
medicine. Dr. Brady practices
psychiatry in Jefferson Parish. The
JOURNAL regrets the error.

JOURNAL VOL 140 JANUARY 5

Crisis in black and white.

Your personal crisis may be waiting in the
morning mail. If so, you’ll want the best
professional help. You’ll want a Medical
Protective General Agent.

Professional liability coverage is our only
business. And we’ve been providing it for
almost 100 years. Our agents live in the
territories they serve so they understand the
local legal climate. And with the extensive

resources of the home office Law Depart-
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answer your questions or give advice.

Someday it may be you against a negligence
charge. When that day comes and your
professional reputation is on the line, you’re
going to want all the help you can get. To
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Protective General Agent today.

1 at ,) t/.MOf a

Dale Weaver

2900 West Fork Drive, Suite 200, Baton Rouge, LA 70827, (504) 291-1807

Norton W. Voorhies, MD, Editor

ECG OF THE MONTH

TOO LONG TO WAIT

JORGE I. MARTINEZ-LOPEZ, MD

The rhythm strip shown below, precordial lead VI, was recorded in a 74-year-old woman shortly after
her admission to the hospital with a clinical diagnosis of acute pancreatitis.

What is your diagnosis? Elucidation is on page 11.

JOURNAL VOL 140 JANUARY 9

PHYSICIANS,
SCHEDULE
SOME TIME FOR
YOUR COUNTRY.

Many physicians would
like to devote some time to their
country in a local Army Reserve
unit. We know that making a
weekend commitment can be
difficult for most physicians. So it
is practical for the Army Reserve
units to be flexible about time.
It’s worth discussing.

Incidentally, in addition
to satisfying your own desire to
serve your country, there are
exceptional opportunities to do
something totally different from
a day-to-day routine. Oppor-
tunities to study new areas of
medicine, meet new people in
your specialty, and be a part of
one of the world ’s most advanced
medical teams.

Discuss the opportunities
with our Army Medical Person-
nel Counselor.

FOR

SURGEONS
LOOKING FOR
ACHAUENGE.

Your challenge could be the
Army Reserve unit near you. It’s a
unit that requires the services of
surgeons.

You may wish to explore the
challenge of teaching in a major
medical center. You may wish to
explore the special challenges of your
specialty in triage. Certainly you’ll be
confronted by challenges very
different from your daily routine.

You’ll also have an opportunity
to participate in a number of pro-
grams in which you’ll be able to
exchange views and information with
other surgeons from all over the
country.

The Army Reserve understands
the time demands on a busy physi-
cian, so you can count on us to be
totally flexible in making time for you
to share your specialty with your
country. We’ll arrange your training
program to work with your practice.

To find out about the benefits of
serving with a nearby Army Reserve
unit, we recommend you call our
Armv Medical Personnel Counselor.

PHYSICIANSJHERE
ARE TWO KINDS
OF FLEXIBILITY IN
THE ARMY RESERVE
WE THINK YOU'LL LIKE.

One, time. We know how
tough it is for a busy physician
to make weekend time commit-
ments. So we offer flexible
training programs that allow a
physician to share some time
with his or her country. We
arrange a schedule to suit your
requirements.

Two, the opportunity to
explore other phases of medi-
cine, to add a different kind of
knowledge— the challenge of
military health care. It’s a flexi-
bility which could prove to be
both stimulating and reward-
ing, with the opportunity to
participate in a variety of
programs that can put you in
contact with medical leaders
from all over the country.

See how flexible we can
be, call our Army Medical
Personnel Counselor.

ARMY RESERVE.
BEAUYOUCANBE.

HERE'S ONE DOCTOR
WHO WON'T PAY
HIS MALPRACTICE
PREMIUMS THIS YEAR.

The Army covers his premiums.
Since he’s an Army Physician, there are
a lot ofworries associated with private
practice that he won’t have tocontend
with. Like excessive paperwork, and the
overhead costs incurred in running a
private practice.

What he will get is a highly challeng-
ing, highly rewardingexperience. The
Armyoffers varied assignments,
chances tospecialize, orfurtheryour
education, and to work with a team of
dedicated health care professionals.

Plus a generous benefits package.

Ifyou'rc interested in practicinghigh
quality health care with a minimum of
administrative burdens, examine Army
medicine. T alk toyourlocal Army
Medical Department Counselor for
more information.

ARMY MEDICINE.
BEAUYOUCANBE.

MAJOR OPPORTUNITIES FOR
HEALTH PROFESSIONALS.

Army/Army Reserve Medicine
144 Elk Place, Suite 1514
New Orleans, LA 701 12
Call collect: (504) 589-2373

ECG of the Month

Case presentation is on page 9.

DIAGNOSIS — Second-degree AV block and ventricular
escape rhythm

The basic cardiac rhythm is sinus at 72 times a minute.

Prominent in the rhythm strip are three impor-
tant features. First, some sinus P waves are con-
ducted, while others are not. Second, two different
types of QRS complexes are present. Third, the tem-
poral relationship of the P waves to the QRS com-
plexes is not constant. The significance of these three
findings will be explored further in the discussion to
follow.

To facilitate the interpretation of the tracing and
the discussion that follows, use the fifth P wave on
the top panel as the point of departure.

DISCUSSION

Sinus rhythm is signaled in the tracing by the regular
appearance of P waves at rates of 72 times a minute.
Ventricular electrical activity, on the other hand, is
characterized by the presence of QRS complexes with
two very different morphologies: one is narrow, neg-
atively oriented, and is followed by a normal T wave;
the other is abnormally wide (0.12 sec), has an rsR'
pattern, and is followed by secondary ST-T wave ab-
normalities.

The P-R interval between the fifth P wave and
the narrow QRS that follows it is normal (0.18 sec).
The next PR interval, however, lengthens to 0.26 sec.
Measurement of subsequent PR intervals reveals that
the interval associated with the seventh P remains at
0.26 sec, while that of the eighth P lengthens to 0.28
sec, and remains unchanged with the ninth and tenth
P waves. In the second panel of the rhythm strip, the
PR interval associated with the first P increases further
to 0.32 sec, and the next P is not conducted. Similar
sequences are recorded throughout the tracing wher-
ever narrow QRS complexes are inscribed. In other
words, sinus P waves keep temporal relationship with
the narrow QRS complexes, but PR intervals pro-
gressively lengthen until a P wave is not conducted.
This pattern is consistent with the ECG diagnosis of
second-degree, Mobitz 1 AV block (or Wenckebach pe-
riodicity). Because the PR intervals lengthen, then

remain static before lengthening again, the pattern
represents a so-called atypical form of Mobitz I AV
block. The three sequences recorded in the tracing
represent AV ratios of 8:7, 11:10, and 9:8 respectively.

Second-degree, Mobitz I AV block is the result
of a conduction disorder at the AV junctional level.
During sinus rhythm, and in the absence of concom-
itant bundle branch block, ventricular complexes are
narrow, denoting normal distal intraventricular con-
duction.

Pauses occasioned by non-conducted sinus P
waves may be interrupted or terminated in several
ways: by the appearance of a subsequent sinus P wave,
ectopic premature impulses, ectopic escape impulses,
or ectopic escape rhythms. The second panel of the
rhythm strip shows four consecutive wide QRS com-
plexes after the non-conducted sinus P. The first of
the four QRS complexes occurs after a long pause
(0.96 sec after the preceding narrow QRS). Therefore,
this wide QRS is not a premature ventricular impulse,
but a ventricular escape impulse. Moreover, the brief
sequence of four consecutive wide QRS complexes
represents a ventricular escape rhythm at rates of 65
times a minute. Other similar sequences are found
throughout the tracing. Of interest is the fact that the
escape interval is not constant; it is either equal to or
longer than the R-R interval during the escape rhythm
(0.76 sec).

The location of the Ps, with respect to the wide
QRS complexes, has no effect on either the escape
interval or the firing rate of the ectopic ventricular
site. This finding provides another ECG diagnosis:
there is A-V dissociation during the sequences of ven-
tricular escape rhythm.

Now, back to the wide QRS complexes. Already
established is the fact that they are caused by a ven-
tricular escape mechanism at rates of 65 times a min-
ute. On this basis, two ventricular rhythms can be
excluded: the ventricular rate is too slow for ventric-
ular tachycardia and too fast for idioventricular
rhythm. The escape rhythm is due to accelerated idio-
ventricular rhythm (AIVR).

Criteria for the ECG diagnosis of AIVR include
the following: 1) ectopic ventricular rhythm with rates
of 50 to 125 times a minute, 2) initiation of the rhythm
by an escape impulse or a fusion beat appearing dur-
ing slowing of the sinus rate or during partial AV
block, 3) a regular R-R interval, and 4) termination
with a return to the basic rhythm, with or without ^

JOURNAL VOL 140 JANUARY 11

YOCON'

YOHIMBINE HCI

Oescriptfim: Yohimbine is a 3a-15a-20B-17a-hydroxy Yohimblne-ISa-car-
boxylic acid methyl ester. The alkaloid is found in Rubaceae and relatedtrees.
Also in Rauwolfia Serpentina (1) Benth. Yohimbine is an indolalkylamine
alkaloid with chemical similar!^ to reserpine. It is a crystalline powder,
odorless. Each compressed tablet contains (1/12 gr.) 5.4 mg of Yohimbine
Hydrochloride.

Actiwi: Yohimbine blocks presynaptic atpha-2 adrenergic receptors. Its
action on peripheral blood vessels resembles that of reserpine, though it is
» weaker arid of short duration. Yohimbine’s peripheral autonomic nervous
system effect Is to increase parasympathetic (cholinergic) and decrease
sympattietlc (adrenergic) activity. It is to be noted that in male sexual
performance, erection is linked to cholinergic activity and to alpha-2 ad-
renergic blockade which may ttteoretically result in increased penile inflow,
decreased penile outflow or both.

Yohimbine exerts a stimulating action on the mood and may increase
anxiety. Such actions have not been adequately studied or related to dosage
although they appear to require high doses of the drug . Yohimbine has a mild
anti-diuretic action, probably via stimulation of hypothalmic centers and
release of posterior pituitary hormone.

Reportedly, Yohimbine exerts no significant influence on card'rac stimula-
tion and other effects mediated by B-adrenergic receptors, its effect on blood
pressure, if any, would be to lower it; however no adequate studies are at hand
to quafrttate this effect irt terms of Yohimbine dosage.

Indications: Yocon® is indicated as a sympathicolytlc and mydriatric. It may
have activity as an aphrodisiac.

Contraindintions: Renal diseases, and patient’s sensitive to Ihe drug. In
view of die limited and inadequate information at hand, no precise tabulation
can be offered of additional contraindications.

VVarnlim: Generally, this drug is not proposed for use in females and certainly
must not be used during pregnancy. Neither is this drug proposed for use in
pediatric, geriatric or cardio-renal patients with gastric or duodenal ulcer
history. Nor should it be used in conjunction with mood-modifying drugs
such as antidepressants, or in psychiatric patients in general.

Adverse Reactions: Yohimbine readily penetrates the (CNS) and produces a
complex pattern of responses in lower doses than required to produce periph-
eral a-adrenergic blockade. These include, anti-diuresis, a general picture of
* central excitation including elevation of blood pressure and heart rate, in-
creased motor activity, irritability and tremor. Sweating, nausea and vomiting
are common after parenteral administration of the drug.^ ^ Also dininess,
headache, skin flushing repotted when used orally, f 3
Dosage and Administration: Experimental dosage reported in treatment of
erectile impotence. T3,4 -| tablet (5.4 mg) 3 times a day, to adult males taken
orally. Occasional side effects reported with this dosage are nausea, dizziness
or nervousness. In the event of side effects dosage to be reduced to Vi tablet 3
times a day. followed by gradual increases to 1 tablet 3 times a day. Reported
therapy not more than 10 weeks. 3
How Applied: Oral tablets of Yocon® 1/12 gr. 5.4 mg in
bottles of 100’s NDC 53159-001-01 and 1000’s ^

53159-001*10. 4" ^^***'^

References;

1. A- Morales et al.. New England Journal of Medi-
cine: 1 221 . November 12 . 1981 .

2. Goodman, Gilman — The Pharmacological basis
of Therapeutics 6th ed , , p . 1 76 - 1 88.

McMillan December Rev. 1/85.

3. Weekly Urological Clinical letter, 27:2, July 4,

1983.

4. A. Morales et al. , The Journal of Urology 128:

45-47, 1982.

Rev. 1/85

AVAILABLE EXCLUSIVELY FROM

PALISADES

PHARMACEUTICALS, INC.

219 County Road
Tenafly, New Jersey 07670

(201) 569-8502
Outside NJ 1-800-237-9083

fusion beats. The morphology of the wide QRS com-
plexes during AIVR is uniform in most instances. On
rare occasions, multiform AIVR (ie, displaying at least
two different QR morphologies) can occur.

The combination of second-degree, Mobitz I
A-V block with AIVR is not a common one. In this
patient, AIVR surfaces when a subsidiary pacemaker
in the ventricular musculature decides that the pause
created by the A-V block is “too long to wait for."
Therefore, the subsidiary pacemaker fires, at times
resulting in a single escape impulse or in a non-sus-
tained burst of AIVR. ■

SELECTED REFERENCES

1. Schamroth L: Idioventricular tachycardia. / Electrocardiol 1968;1:205-212.

2. Rothfeld EL, Zucker IR: Multiform accelerated idioventricular rhythm.
Angiology 1974;25:457-461.

3. Sclarovsky S, Strasberg B, Martonovich G, et al: Ventricular rhythms with
intermediate rates in acute myocardial infarct. Chest 1978;74:180-182.

4. Sclarovsky S. Strasberg B, Fuchs J, et al: Multiform accelerated idioven-
tricular rhythm in acute myocardial infarction. Am } Cardiol 1983;52:43-47.

Dr. Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Department of Medicine at
William Beaumont Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Department of the Army or Department of Defense.

12 JOURNAL VOL 140 JANUARY

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

STRIDOR IN INFANTS AND CHILDREN

J. LINDHE GUARISCO, MD; H. DEVON GRAHAM III, MD;

HENRY A. MENTZ III, MD

Stridor is a sign of upper airway obstruction.
Though it may be associated with a benign
disorder, it may be the initial sign of a life-
threatening disease. The various congenital and
acquired etiologies of stridor in infants and
children are reviewed. Key diagnostic and
therapeutic measures are briefly discussed.

S TRIDOR IS AiN abnormally harsh respiratory sound
of variable pitch produced by turbulent airflow
through a partial obstruction. It may occur as a result
of obstruction in any portion of the upper airway.
Though stridor may be the result of a relatively benign
process, it is often the initial sign of a serious and
even life-threatening disorder. It is the purpose of this
paper to review some of the more common etiologies
of upper airway obstruction in infants and children
and briefly outHne a rational diagnostic and thera-
peutic approach to the problem.

ANATOMY

The upper airway begins at the nares and lips and
ends with the secondary bronchi. It is convenient for
diagnostic purposes to divide the upper airway into
three different anatomic regions. These are the su-
praglottic airway, the subglottic-extrathoracic airway,
and the subglottic-intrathoracic airway. The supra-
glottic airway includes the nose, oral cavity, naso-
pharynx, oropharynx, hypopharynx, and supraglottic
larynx. The subglottic-extrathoracic airway includes
the glottis (vocal cords and 1 cm below), subglottis
(cricoid ring), and cervical trachea. The subglottic-

JOURNAL VOL 140 JANUARY 13

TABLE 1

CONGENITAL ETIOLOGIES

I. Anatomic

1 ) Choanal atresia

2) Micrognathia (Treacher-Collins)

3) Macroglossia (Beckwith-Wiedemann)

4) Thyroglossal duct cyst

5) Lingual thyroid

6) Laryngomalacia

7) Laryngoceles

8) Laryngeal webs

9) Vocal cord paralysis

1 0) Vocal cord cysts

1 1 ) Subglottic stenosis

12) Subglottic hemangioma

13) Vascular compression (aberrant innominate)

14) Tracheal stenosis

15) Tracheomalacia

16) Esophageal duplication cysts

17) Bronchial stenosis

18) Bronchogenic cysts

19) Others

II. Infectious

1) Syphilis

2) Herpes

3) Others

III. Neoplasms

1) Teratoma

2) Neuroblastoma

3) Hemangioma

4) A-V malformations

5) Others

IV. Neurologic

1) CNS malformation

2) Hypoxic encephalopathy

3) Others

intrathoracic airway is made up of the intrathoracic
trachea and the mainstem, primary and secondary
bronchi.^ By using this anatomic classification and lo-
calizing the origins of the stridor through careful his-
tory and physical examination, the differential diag-
nosis may be greatly narrowed.

PATHOPHYSIOLOGY

Stridor may be the result of any of four patho-
physiologic mechanisms. Intraluminal lesions, extrin-
sic abnormalities leading to airway compression, and
diseases leading to mucosal thickening or smooth
muscle contraction may all result in stridor. In chil-
dren minimal changes in airway diameter may lead

14 JOURNAL VOL 140 JANUARY

to significant airway compromise. This is demon-
strated by Poiseuille's law which, in effect, states that
the resistance of the airway is inversely proportional
to the fourth power of the radius. For example, if the
radius of the airway is decreased by 1 mm (from 3
mm to 2 mm), a fivefold increase in driving pressure
is necessary to maintain airflow. As the changing
pressure increases, an additional physiologic princi-
ple, known as the Venturi principle, comes into play.
This states that linear movement of a gas creates a
drop in pressure at a vector 90° to the vector of gas
movement. Therefore, in our previous example, as
driving pressure is increased, the airway waUs tend
to collapse inward.^

ETIOLOGY

There are numerous congenital and acquired causes
of upper airway obstruction. The most common con-
genital disorders leading to stridor are anatomic mal-
formations of the upper airway. Congenital infec-
tions, neoplasms, and neurologic disorders may also
involve the upper airway and lead to varying degrees
of obstruction. The most common acquired etiologies
of stridor are infectious diseases. Other acquired etiol-
ogies include allergic, neoplastic, traumatic, neuro-
logic, and idiopathic inflammatory disorders of the
upper airway. Tables 1 and 2 list some of the more
common causes of congenital and acquired upper air-
way obstruction.^'^

MANAGEMENT

The evaluation of a child with stridor should ob-
viously begin with a careful history and physical ex-
amination. Clues to specific congenital and acquired
disorders are easily obtained with proper questioning.
The past medical history is important. Any prior his-
tory of intubation, airway instrumentation, or airway
trauma is especially relevant. The physical exam
should include a complete set of vital signs and height
and weight measurements. The anthropometric
measurements are very important in evaluating a child
with chronic stridor. For example, a young child with
chronic low-grade obstruction secondary to tonsil and
adenoid hypertrophy with height and weight in the
less than fifth percentile has a serious disorder re-
quiring surgical intervention. The nose, mouth, oral
cavity, nasopharynx, oropharynx, hypopharynx, and
larynx must be carefully inspected. The flexible fi-

beroptic endoscope facilitates an excellent office ex-
amination of the upper airway to the level of the glot-
tis. Auscultation of the upper airway, as weU as the
lung periphery, will give reliable clues to the site of
the abnormality. The remainder of the physical ex-
amination must not be neglected as valuable clues to
systemic disease may be overlooked.

Basic laboratory and radiographic studies may aid
in diagnosis. Lateral and AP neck films and inspira-
tory and expiratory chest films may be very useful.

A complete blood count with differential count, a
monospot, Epstein-Barr virus titers, throat and blood
cultures, and latex agglutination studies on blood and
urine may assist in determining a specific infectious
etiology. Special laboratory and radiographic tests are
ordered as necessary. High resolution computed to-
mography scanning and xeroradiographs of the upper
airway are often very helpful. The final step in di-
agnosis is rigid endoscopy. This is required to verify
lesions at or below the level of the vocal cords.

The most important aspect of treating a child with
stridor is to ensure an adequate airway. In certain
instances, emergency measures must be undertaken
as the initial phase of management prior to complet-
ing the history and physical. After the airway has
been properly secured, additional therapy is insti-
tuted. Supportive measures include intravenous fluids,
humidification, O2, suctioning, proper positioning,
and aerosol treatments. Disease specific measures are
instituted as indicated. Medical therapy most often
involves the use of steroids and antibiotics. Medical
treatment of certain allergic, neoplastic, and idi-
opathic inflammatory disorders usually requires the
expertise of the appropriate consultant.^

Surgical therapy may initially involve tracheot-
omy to bypass a life-threatening obstruction. Excision
of neoplasms, repair of airway trauma, reconstruction
of the larynx and trachea, removal of foreign bodies,
adenotonsiUectomy, anti-reflux surgery, and other
procedures are recommended as indicated.

SUMMARY

Stridor, a sign of upper airway obstruction, has nu-
merous congenital and acquired etiologies, many of
which are life threatening. A meticulous approach to
the history and physical examination, including flex-
ible fiberoptic endoscopy, will facilitate proper diag-
nosis. Basic and special laboratory tests are often use- ►

TABLE 2

ACQUIRED ETIOLOGIES

I. Infectious

1) Purulent rhinitis

2) Ludwig’s angina

3) Tonsillitis

4) Peritonsillar abscess

5) Retropharyngeal abscess

6) Epiglottitis

7) Laryngotracheobronchitis (viral croup)

8) Bacterial tracheitis

9) Bacterial bronchitis

10) Viral bronchitis

11) Others

II. Allergic

1) Allergic rhinitis

2) Hereditary angioneurotic edema

3) Anaphylaxis

4) Others

III. Neoplasms

1) Papilloma

2) Hemangioma

3) Lymphangioma

4) Lymphoma

5) Rhabdomyosarcoma

6) Cystic hygroma

7) Others

IV. Trauma

1) Facial fractures

2) Lingual hematoma (hemophiliacs)

3) Retropharyngeal hematoma (cervical spine injury)

4) Laryngotracheal fractures

5) Inhalation or ingestion injuries

6) Intubation injury (subglottic stenosis, subglottic
granuloma)

7) Others

V. Neurologic disorders

1) Loss of innervation and/or coordination of upper
aerodigestive tract muscles with pooling of
secretions and aspiration

VI. Idiopathic inflammatory

1) Wegener’s granulomatosis

2) Relapsing polychondritis

3) Juvenile rheumatoid arthritis (fixation of arytenoids)

4) Others

VII. Others

1) Foreign bodies

2) Tonsil and adenoid hypertrophy

3) Gastroesophageal reflux

4) Psychogenic

JOURNAL VOL 140 JANUARY 15

ful. Rigid endoscopy is usually necessary to confirm
the diagnosis if the obstruction is at or below the level
of the vocal cords. Treatment includes proper sup-
portive and disease specific measures. The most im-
portant aspect of management is the protection of the
airway. ■

REFERENCES

1. Richardson MA, Cotton RJ: Anatomic abnormalities of the pediatric air-
way. Pediatri Clin North Am 1984;31:821-834.

2. Barnes SD, Grob CS, Lachman BS, et al: Psychogenic upper airway ob-
struction presenting as refractory wheezing. / Pediatr 1986;109:1067-1070.

3. Hen J: Current management of upper airway obstruction. Pediatr Ann
1986;15:274-294.

4. Holinger PH, Brown CT: Congenital webs, cysts, laryngoceles and other
anomalies of the larynx. Ann Otol Rhinol Laryngol 1967;76:744-752.

5. Holinger LD: Etiology of stridor in the neonate, infant and child. Ann
Otol Rhinol Laryngol 1980;89:397-400.

6. Orenstein SR, Orenstein DM, Washington PF, et al: Gastroesophageal
reflux causing stridor. Chest 1983;84:301-302.

7. Rychman J, Rodgers BM: Obstructive airway disease in infants and chil-
dren. Surg Clin North Am 1985;65:1663-1687.

Dr. Guarisco is from the Dept of Otolaryngology, Section on Pediatric
Otolaryngology at Ochsner Clinic and Alton Ochsner Medical
Foundation in New Orleans. He is also affiliated with the Dept of
Otolaryngology at Tulane Medical Center in

New Orleans.

Drs. Graham and Mentz are from the Dept of Otolaryngology at
Tulane Medical Center in New Orleans.

Requests for reprints should be sent to Dr ]. Lindhe Guarisco,
Department of Otolaryngology, Section on Pediatric Otolaryngology,
Ochsner Clinic, 1514 Jefferson Hwy, New Orleans, LA 70121.

OlRAFATE'

(sucralfate)

BRIEF SUMMARY

CONTRAINDICATIONS

There are no known contraindications to the use of sucralfate.

PRECAUTIONS

Duodenal ulcer is a chronic, recurrent disease. While short-term treatment
with sucralfate can result in complete healing of the ulcer, a successful
course of treatment with sucralfate should not be expected to alter the
post-healing frequency or severity of duodenal ulceration.

Drug Interactions: Animal studies have shown that the simultaneous
administration of CARAFATE with tetracycline, phenytoin, or cimetidine will
result in a statistically significant reduction in the bioavailability of these
agents. This interaction appears to be nonsystemic in origin, presumably
resulting from these agents being bound by CARAFATE in the gastrointesti-
nal tract. The bioavailability of these agents may be restored simply by
separating the administration of these agents from that of CARAFATE by
two hours. The clinical significance of these animal studies is yet to be
defined.

Carcinogenesis, Mutagenesis, Impairment of Fertility: No evi-
dence of drug-related tumorigenicity was found in chronic oral toxicity
studies of 24 months' duration conducted in mice and rats at doses up to 1
gm/kg (12 times the human dose). A reproduction study in rats at doses up
to 38 times the human dose did not reveal any indication of fertility impair-
ment. Mutagenicity studies have not been conducted.

Pregnancy: Pregnancy Category B. Teratogenicity studies have been
performed in mice, rats, and rabbits at doses up to 50 times the human dose
and have revealed no evidence of harm to the fetus due to sucralfate. There
are, however, no adequate and well-controlled studies in pregnant women.
Because animal reproduction studies are not always predictive of human
response, this drug should be used during pregnancy only if clearly needed.

Nursing Mothers: It is not known whether this drug is excreted in
human milk. Because many drugs are excreted in human milk, caution
should be exercised when sucralfate is administered to a nursing woman.

Pediatric Use: Safety and effectiveness in children have not been
established.

ADVERSE REACTIONS

Adverse reactions to sucralfate in clinical trials were minor and only rarely led
to discontinuation of the drug. In studies involving over 2,500 patients,
adverse effects were reported in 121 (4.7%). Constipation was the most
frequent complaint (2.2%). Other adverse effects, reported in no more than
one of every 350 patients, were diarrhea, nausea, gastric discomfort, indi-
gestion, dry mouth, rash, pruritus, back pain, dizziness, sleepiness, and vertigo.

DOSAGE AND ADMINISTRATION

The recommended adult oral dosage for duodenal ulcer is 1 gm four times a
day on an empty stomach.

Antacids may be prescribed as needed for relief of pain but should not
be taken within one-half hour before or after sucralfate.

While healing with sucralfate may occur during the first week or two,
treatment should be continued for 4 to 8 weeks unless healing has been
demonstrated by x-ray or endoscopic examination.

HOW SUPPLIED

CARAFATE (sucralfate) 1-gm pink tablets are supplied in bottles of 100 and
in Unit Dose Identification Paks of 100. The tablets are embossed with
MARION/1712. Issued 3/84

References:

1. Korman MG, Shaw RG, Hansky J, et al: Gastroenterology 80:1451-1453,
1981.

2. Korman MG, Flansky J, Merrett AC, etal: D/g D/s 5c/ 27:71 2-71 5, 1982.

3. Brandstaetter G, Kratochvil P: Am J Med 79(suppl 2C):36-38, 1985.

4. Marks IN, Wright JR Gilinsky NH, et al: J Clin Gastroenterol 8:419-423,
1986.

5. Lam SK, Hui WM, Lau WY, et al: Gastroenterology 92:1 193-1201, 1987.

Another patient benefit product Irom

— PHARMACEUTICAL DIVISION

MARION

16 JOURNAL VOL 140 JANUARY

1594H7

When brain and bowel conflict

Iflstiitie

the Peacemaker.

In irritable bowel syndrome* anxiety can aggravate intestinal symptoms, which may
further intensify anxiety — a distressing cycle of brain/bowel conflict. Librax intervenes with
two well-known compoimds. The Librium® (chlordiazepoxide HCl/Roche) component
safely relieves anxiety. And Quarzan® (cHdinium bromide/Roche) provides antisecretory
and antispasmodic action to relieve discomfort associated with intestinal hypermotility.

Dual action — for peace between brain and bowel. Because of possible CNS effects, caution
patients about engaging in activities requiring complete mental alertness. Specify Adjimctive

LIBR^

Each capsule contains 5 mg chlordiazepoxide HCl
and 2.5 mg clidinium bromide

*Librax has been evaluated as possibly effective as adjunctive therapy in the treatment of peptic ulcer and the irritable bowel syndrome.
Copyright © 1987 by Roche Products Inc. All rights reserved. Please see summary of prescribing information on adjacent page.

CALENDAR

February

Febraary 4-6

Third International Conference on Monoclonal Antibody
Immunoconjugates for Cancer, San Diego. Contact: Office of
Continuing Medical Education, M-017, University of California
San Diego School of Medicine, La Jolla, CA 92093; (619)534-3940.

February 5-8

Terminal Care: Consultations on Clinical and Policy Pro-
blems, Hilton Head, South Carolina. Penny B. Weingarten,
Program Coordinator, Concern for Dying, 250 West 57th St, Room
829, New York, NY 10107; (800)248-2122.

February 6-13

Infectious & Toxicologic Emergencies, Snowbird Resort,
Snowbird, Utah. Contact: Edith S. Bookstein, Conference
Management Associates, PO Box 2586, La Jolla, CA 92038;
(619)454-3212.

February 9-12

Update Yoiu- Pediatrics-1988, New Orleans. Contact: J.A.
D'Angelo Jr, Office of Continuing Education, Tulane University
Medical Center, 1430 Tulane Ave, New Orleans, LA 70112-2699;
(504)588-5466.

February 11-13

Second Annual UCSD-Sharp Memorial Hospital Interna-
tional Cardiac Symposium, San Diego. Contact: Office of Con-
tinuing Medical Education, M-017, Univeristy of California San
Diego School of Medicine, La Jolla, CA 92093; (619)534-3940.

February 11-13

Vascular Surgery Course, New Orleans. Contact: Alton
Ochsner Medical Foundation, 1516 Jefferson Hwy, New Orleans,
LA 70121; (504)838-3702.

February 11-13

Mardi Gras Endocrinology Update, New Orleans. Contact:
Alton Ochsner Medical Foundation, 1516 Jefferson Hwy, New
Orleans, LA 70121; (504)838-3702.

February 13-15

Mardi Gras Anesthesia Update, New Orleans. Contact: J.A.
D'Angelo Jr, Office of Continuing Education, Tulane University
Medical Center, 1430 Tulane Ave, New Orleans, LA 70112-2699;
(504)588-5466.

February 15-17

Recent Advances in Geriatric Rehabilitation 1988: What Is

It? Who Needs It? What Works?, San Diego. Contact: Office
of Continuing Medical Education, University of San Diego School
of Medicine, La Jolla, CA 92093; (619)534-3940.

February 16-21

The Fundamentals of Plastic Surgery— The Basics in Perspec-
tive, Snowbird Ski & Summer Resort, Snowbird, Utah. Con-
tact: American Society of Plastic and Reconstructive Surgeons, 233
N Michigan Ave, Suite 1900, Chicago, IL 60601; (312)856-1818.

February 20-22

New Orleans Academy of Ophthalmology 37th Aimual
Symposium on What's New in Ophthalmology, New

Orleans. Contact: Emily Busby, Executive Secretary, Eye, Ear,
Nose & Throat Hospital, 145 Elk Place, Room 203, New Orleans,
LA 70112.

February 20-27

Duke at Vail: Frontiers in Dermatology and Rheumatology,

Vail, Colorado. Contact: Angelika Langen, Box 3135, Duke
University Medical Center, Durham, NC 27710; (919)684-2504.

February 20-27

Pediatric Emergencies, Royal Lahaina Resort, Maui, Hawaii.
Contact: Edith S. Bookstein, Conference Management Associates,
PO Box 2586, La Jolla, CA 92038; (619)454-3212.

February 22-26

Physician in Management-Seminar I, The Royal Plaza at
Disney World, Orlando, Florida. Contact: Sherry Mason,
American Academy of Medical Directors, 4830 W Kennedy Blvd,
Suite 648, Tampa, FL 33609-2517; (813)287-2000.

February 24-26

Aestetic and Reconstructive Rhinoplasty— What's New in
Plastic Surgery?, Manzanillo, Colima, Mexico. Contact: Juanita
Navarette, Division of Plastic & Reconstructive Surgery, Har-
bor/UCLA Medical Center, 1000 W Carson St, Torrance, CA
90509; (213)533-2760.

February 25-27

Second International Conference on Intracavitary
Chemotherapy, San Diego. Contact: Office of Continuing
Medical Education, M-017, University of California San Diego
School of Medicine, La Jolla, CA 92093; (619)534-3940.

February 26-27

Arrhythmias: Interpretation, Diagnosis and Management,

New Orleans. Contact: Medical Education Resources, 5808 S Rapp
St, Suite 202, Littleton, CO 80120; (800)421-3756, (303)798-9682.

22 JOURNAL VOL 140 JANUARY

February 26-28

Rhinoplasty: An Educational Symposium, Dallas. Contact:
Continuing Education, The University of Texas Health Science
Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75235;
(214)688-2166.

February 28 - March 4

Annual Meeting of the United States and Canadian
Academy of Pathology, Washington, DC. Contact: Dr. Nathan
Kaufman, Building C, Suite B, 3515 Wheeler Road, Augusta, GA
30909; (404)733-7550.

March

March 6-11

9th Annual Mammoth Mountain Emergency Medicine,

Mammoth Lakes, California. Contact: Medical Conferences, Inc,
CME Travel Service, 1615 S Mission Road, Suite 3, Fallbrook, CA
92028; (714)650-4156.

March 7-9

j World Congress III on Cancers of the Skin, The Lincoln
I Hotel Post Oak, Houston. Contact: University of Texas M.D.

I Anderson Hospital and Tumor Institute, Office of Conference Ser-
j vices HMB 131, 1515 Holcombe Blvd, Houston, TX 77030;

\ (713)792-2222.

1988 Annual Meeting
Louisiana State Medical Society
March 10-13, Lake Charles

March 12-27

Australia/New Zealand - Diagnostic Imaging Down Under,

Australia and New Zealand. Contact: Medical Seminars Inter-
national, 21915 Roscoe Blvd, Suite 222, Canoga Park, CA 91304;
(818)719-7380.

March 14-18

2nd Annual Update on Primary Care, Steamboat Springs,
Colorado. Contact: Larry G. McLain, MD, Dept of Pediatrics,
Loyola University Medical Center, 2160 South First Ave,
Maywood, Illinois 60153; (312)531-3195.

March 16-19

Highlights in Women's Health Care, Orlando, Horida. Con-
tact: Susan Larson, Director, Scott and White Office of Continu-
ing Medical Education, 2401 South 31st St, Temple, TX 76508;
(817)774-4083.

March 17-18

Assessment of Clinical Competence in Specialty Medicine,

Toronto Hilton Harbour Castle Hotel, Toronto. Contact:
American Board of Medical Specialties, One Rotary Center #805,
Evanston, IL 60201.

March 17-20

Hair Replacement Surgery, Los Angeles. Contact: American
Academy of Facial Plastic and Reconstructive Surgery, 1101 Ver-
mont Ave NW, Suite 404, Washington, DC 20005.

JOURNAL VOL 140 JANUARY 23

Sancy H. McCool, LSMSA President H

AUXILIARY REPORT

LONG-RANGE PLANNING

MARILYN S. CANALE

A S AN ADVISORY COMMITTEE to the Louisiana State
Medical Society Auxiliary, the Long-Range Plan-
ning Committee has the duty to study and evaluate
present programs and procedures, and make deci-
sions now in order to avoid escalating problems that
will necessitate hasty decisions in the future. Sec-
ondly, the Committee looks at the future objectives
and growth, and developing programs and goals by
using available resources.

The Long-Range Planning Committee must be
selected carefully, with consideration for continuity
and experience. Two of the current members. Opal
McBride and Lorre Lei Jackson, are former state pres-
idents and Long-Range Planning chairmen. Christy
Maraist, Martha Maxwell and Christy Owens were
selected for their past, and current, involvement in
health and fund-raising activities and membership.
The members of the Committee are also representa-
tive of the entire membership, reflecting all age groups
and geographical areas of the state.

The first step in long-range planning is to estab-
lish an information base of overall objectives. Last
year's Committee evaluated present programs by
means of an internal survey of each parish auxiliary.

24 JOURNAL VOL 140 JANUARY

Every facet of auxiliary work and involvement was
covered. The internal analysis showed "work, enthu-
siasm and community involvement reflecting a
strengthening community service organization."

Change and growth were evident in the health
programs. More auxiliaries are now addressing pro-
grams involving children, such as child abuse pro-
tection, youth suicide, child care and health and chil-
dren health fairs.

The rapport between the state and parish medical
societies and the state and parish medical society aux-
iliaries has been growing each year. Auxilians
throughout the state respond to the call for legislative
alerts and two auxilians sit on the board of their parish
societies. Programs for membership were innovative
and productive. Antique shows, style shows, sharing
cards and a golf tournament all combined to raise over
$60,000 for Louisiana medical schools.

The Long-Range Planning Committee, after es-
tablishing the information base, is now identifying
basic problems and opportunities by examining our
state administrative policy and functions. Questions
and perceived problems have been sent to the chair-
men and they are now in the process of being studied

and reviewed by the Committee. Short- and long-
term objectives and programs are being developed.
Actionable objectives, which are those that we can do
something about, include the allocation and dispo-
sition of funds for the Annual Meeting. It has been
recognized that times and circumstances change, and
that auxiliary policies must be flexible enough to ac-
commodate these changes. The Committee is also
evaluating the establishment of criteria guidelines for
the selection of honored guests, guidelines for the
responsibilities of the president and president-elect,
and the eligibility requirements as they are now writ-
ten. Questions concerning membership delegate
count, and the lack of uniformity among parish, state,
and national membership deadline dates are being
thoughtfully and carefully studied.

Recommendations have been made to the Aux-

iliary to stimulate decisions that will contribute to the
growth of the Auxiliary. The Long-Range Planning
Committee has analyzed where the Auxiliary is now,
on the parish level and, administratively, on the state
level. There are short-range goals developed for the
coming year, and long-range goals for future years.
Some questions are already answered, some solutions
already in place. Other questions have been directed
to the Executive Committee with recommendations
or will be addressed by the serious effort of an ad hoc
committee. This is Long-Range Planning — an on-
going process to fulfill goals, present and future. ■

Mrs. Canale (wife of Dr. Thomas J. Canale) is chairman of the Long-
Range Planning Committee of the LSMS Auxiliary.

Timberlawn Psychiatric Hospital

E.stablished in 1917
Children • Adolescents • Adults

• 232 Inpatient Beds • Substance Abuse Services

• Outpatient Services Inpatient and Outpatient Programs

• Panial Hospitalization Programs Health Professionals Program

• Residential Services Residential After Care

• Departments of Psychology, • Psychiatric Residency’ Training Program

Neuropsychology and Social Work • Child Residenq’ Training Program

• Family Assessment and Treatment • JCAH Approved

Admissions: RO. Box 11288 Dallas, Texas 75223 214/381-7181

JOURNAL VOL 140 JANUARY 25

ANNOUNCING

Convenient 500-mg b.i.d.
dosage and demonstrated
effectiveness for
treatment of:

□ skin and skin structure infections*

□ uncomplicated cystitis^

□ pharyngitis*

• New hydrochloride salt form of cephalexin—
requires no conversion in the stomach before
absorption

• Well-tolerated therapy

• May be taken without regard to meals

For other indicated infections, 250-mg tablets available
for q. id. dosage

Priced less than Keflex®cephaiexin)

Keftab is contraindicated in patients with known allergy to the
cephalosporins and should be given cautiously to penicillin-
sensitive patients.

Penicillin is the drug of choice in the treatment and prevention
of streptococcal infections, including the prophylaxis
of rheumatic fever.

KEFTAB™

(cephalexin hydrochloride monohydrate)

Summary: Consult the package literature for
prescribing information.

Indications and Usage:

Respiratory tract infections caused by susceptible
strains of Streptococcus pneumoniae and group A
iS-hemolytic streptococci.

Skin and skin structure infections caused by sus-
ceptible strains of Staphylococcus aureus and/or
jS-hemolytic streptococci.

Bone infections caused by susceptible strains of
S aureus and/or Proteus mirabilis.

Genitourinary tract infections, including acute prosr
tatitis, caused by susceptible strains of Escherichia
coli, P mirabilis, and Klebsiella sp.

Contraindication: Known allergy to cephalosporins.

Warnings: KEFTAB SHOULD BE ADMINISTERED
CAUTIOUSLY TO PENICILLIN-SENSITIVE PA-
TIENTS. PENICILLINS AND CEPHALOSPORINS
SHOW PARTIAL CROSS-ALLERGENICITY. POSSI-
BLE REACTIONS INCLUDE ANAPHYLAXIS.
Administer cautiously to allergic patients.
Pseudomembranous colitis has been reported with
virtually all broad-spectrum antibiotics. It must be
considered in differential diagnosis of antibiotic-
associated diarrhea. Colon flora is altered by broad-
spectrum antibiotic treatment, possibly resulting in
antibiotic-associated colitis.

Precautions:

• Discontinue Keftab in the event of allergic reac-
tions to it.

• Prolonged use may result in overgrowth of nonsus-
ceptible organisms.

• Positive direct Coombs' tests have been reported
during treatment with cephalosporins.

• Keftab should be administered cautiously in the
presence of markedly impaired renal function. Al-
though dosage adjustments in moderate to severe
renal impairment are usually not required, careful
clinical observation and laboratory studies should
be made.

• Broad-spectrum antibiotics should be prescribed
with caution in individuals with a history of gas-
trointestinal disease, particularly colitis.

• Safety and effectiveness have not been determined
in pregnancy and lactation. Cephalexin is excreted
in mother’s milk. Exercise caution in prescribing
Keftab for these patients.

• Safety and effectiveness in children have not been
established.

Adverse Reactions:

• Gastrointestinal, including diarrhea and, rarely, nau-
sea and vomiting. Transient hepatitis and chole-
static jaundice have been reported rarely.

• Hypersensitivity \n the form of rash, urticaria, angio-
edema, and, rarely, erythema multiforme, Stevens-
Johnson syndrome, or toxic epidermal necrolysis.

• Anaphylaxis has been reported.

• Other reactions have included genital/anal pruri-
tus, genital moniliasis, vaginitis/vaginal discharge,
dizziness, fatigue, headache, eosinophilia, neutro-
penia, and thrombocytopenia; reversible interstitial
nephritis has been reported rarely.

• Cephalosporins have been implicated in trigger-
ing seizures, particularly in patients with renal
impairment.

• Abnormalities in laboratory test results included
slight elevations in aspartate aminotransferase
(AST, SCOT) and alanine aminotransferase (ALT,
SGPT). False-positive reactions for glucose in the
urine may occur with Benedict’s or Fehling’s solu-
tion and Clinitest® tablets but not with Tes-Tape®
(Glucose Enzymatic Test Strip, USP, Lilly).

"'Due to susceptible strains of Staphylococcus aureus and/or /3-hemolytic streptococci.
■ Due to susceptible strains of Escherichia coli, Proteus mirabilis. and Klebsiella sp,

’ Due to susceptible strains of group A /3-hemolytic streptococci.

PV 2060 DPP [091887]

849336

TRAUMATIC OCCUPATIONAL
OCCLUSIVE ARTERIAL DISEASE
OF THE HANDS

TERRY R. JONES, MD; JOHN D. FRUSHA, MD;
JON V. SCHELLACK, MD

28 JOURNAL VOL 140 JANUARY

Hypothenar hammer syndrome occurs following
ulnar artery occlusion or aneurysm formation
resulting from repetitively using the hypothenar
area of the hand to hammer, strike, push, or twist
hard objects. Vibration syndrome occurs from the
use of vibrating tools and results in Raynaud's
phenomenon or even digital gangrene. Although
the hypothenar hammer syndrome and the
vibration syndrome are not well publicized, they
have important implications to vocational
disability. A case report is presented and the

syndromes discussed.

P ATIENTS WITH unilateral upper extremity ischemia
or Raynaud's phenomenon should have a careful
history and physical to determine if their arterial prob-
lem may be related to occupational trauma. Failure to
discover this possibility may deprive patients of right-
ful disability compensation or result in less than op-
timal medical management.

We have treated several patients with occupa-
tion-caused ischemia of the upper extremity and have
found that some insurance companies were unfamil-
iar with these syndromes. In one current textbook,
devoted entirely to upper extremity vascular disor-
ders, less than a single paragraph is devoted to hy-
pothenar hammer syndrome,^ and in one review of
500 articles in the world literature on vibration syn-
drome, only 15 were in the American literature.^ We
present a case which illustrates both these conditions.

CASE REPORT

A 53-year-old right-handed white male electrician de-
veloped pain, paresthesias, and discoloration of his
right hand several hours after using it to repeatedly
slam conduit pipe across a box in an effort to bend
the pipe. His work also involved daily use of a vi-
brating tool called a rotary hammer, and he admitted
using his hand regularly to strike objects. He sought
medical attention several days later and was started
I on nifedipine. Ischemic signs and symptoms pro-
j grossed and he was referred for vascular surgery eval-
uation.

Physical examination disclosed bluish mottling of
i the hypothenar eminence of the hand and obvious
ischemia of digits 2-5 but no apparent abnormality of
his thumb. A transfemoral arch aortogram and selec-

Fig 1. Arteriogram showing occlusion of most of
the superficiai and deep paimer arterial
arches.

tive brachial arteriogram (Fig 1) was done; demon-
strated was occlusion of the distal ulnar artery and
the superficial palmar arch. The patient underwent
streptokinase therapy with subsequent clearing of the
mottling of his hypothenar eminence and restoration
of carpal arch blood flow. His digital flow was im-
proved but ischemia persisted. He was started on
dextran, nifedipine, and pentoxifylline, with further
improvement. He was discharged on aspirin, nifed-
ipine, and pentoxifylline. Several weeks later his hand
appeared normal. The nifedipine and pentoxifylline
were tapered and discontinued with no exacerbation
of ischemic signs or symptoms. Nine months later,
on a follow-up visit, he complained of cold sensitivity
in his right hand and reported temporary paresthesias
when he tried to use a hammer. He was considered
totally disabled to perform his usual work and a vo-
cation change was recommended.

DISCUSSION

The term "hypothenar hammer syndrome" was first
used by Conn, et al in 1970 to describe the ulnar artery
occlusion that resulted from repetitive blunt trauma
to the hand.^ Individuals using the hypothenar area
of their hand to hammer, strike, push, or twist hard
objects can injure the ulnar artery against the hook
of the hamate wrist bone (Fig 2). The syndrome has ►

JOURNAL VOL 140 JANUARY 29

Fig 2. Diagram iiiustrating how uinar artery may be
impacted against hook of hamate carpai bone
from direct pressure to hypothenar emin-
ence of the hand.

a high incidence in auto mechanics and electricians
but can occur in any situation in which the hand is
misused, such as by devotees of the martial arts and
by patients who lean on canes or crutches.

This syndrome probably occurs more frequently
than is reported due to the reluctance of patients to
seek medical assistance for a problem that threatens
termination of their jobs. In one survey of 127 vehicle
maintenance workers, 79 admitted to using their hands
as a hammer on a regular basis. Eleven of these 79

men (14%) exhibited signs and symptoms of the hy-
pothenar hammer syndrome, and yet they had not
sought medical attention.^

Other reasons for the failure to recognize this
syndrome are the apparent triviality of the respon-
sible injury or misdiagnosis of the condition.^ The
differential diagnosis includes Raynaud's disease,
Raynaud's phenomenon associated with connective
tissue disease, direct trauma to the fingers, ischemia
from emboli secondary to proximal disease, primary
occlusive vascular disease, chemical poisonings, dys-
globulinemias, blood dyscrasias, and neurologic
causes.

The symptoms may be quite variable, producing
from no symptoms or just intermittent paresthesias
to the full clinical picture of Raynaud's phenomenon
or gangrene. One reason for the variability of symp-
toms is the variability in the anatomy of the normal
hand. The ulnar artery usually terminates as the su-
perficial palmar arch from which the palmar digital
arteries arise. However, this arch is complete in only
70% of individuals.®' ^ Although the fourth and fifth
digits are most commonly involved in hypothenar
hammer syndrome (HHS), any digit can be involved
because of this variability in blood supply.

The diagnosis of HHS can be strongly suspected
when Raynaud's phenomenon appears in the domi-
nant hand of a male worker who has used his hands
repetitively to strike hard objects. In one large series
of 966 patients with Raynaud's phenomenon, there
was a 1.7% incidence of HHS.® The syndrome occurs
rarely in women. It can occur bilaterally. Occasionally
the ulnar artery injury will result in an aneurysm which
can be palpatead as a pulsatile mass near the wrist.
If the aneurysm has thrombosed, the mass must be
differentiated from ganglion cyst or tumor. Usually,
HHS does not involve the thumb and does not exhibit
neurological symptoms or hyperemia. Arteriog-
raphy is required for definitive diagnosis, to exclude
other disease, and to delineate the anatomy and ex-
tent of involvement so that an adequate treatment
plan may be formulated.

Treatment consists of resection of the ulnar artery
aneurysm, if present, and reconstruction of the ulnar
artery. If no aneurysm is present, conservative man-
agement is recommended since the prognosis is ex-
cellent once the causative trauma has been discontin-
ued.

Vibration syndrome is a term used to describe

30 JOURNAL VOL 140 JANUARY

the symptoms of Raynaud's phenomenon in workers
who use vibrating tools and who have no other etiol-
ogy for the phenomenon. The syndrome is known
variously as Raynaud's phenomenon of occupational
origin, vibration-induced white finger, traumatic
vasospastic disease, dead finger, and dead hand.^ Un-
like HHS, vibrating syndrome may exhibit neurolog-
ical symptoms or produce orthopedic complications
such as osteoarthritis at the wrist or shoulders, carpal
bone cysts, or olecranon exostoses.

The incidence and recognition of vibratory syn-
drome is greater than that of the HHS. In one survey,
the vibration syndrome was shown to occur to some
degree in 89% of American stonecutters^^ and, in an-
other survey, in 79% of shipyard caulkers. The vi-
bration syndrome also has a high incidence in forest
workers who use chain saws, although improve-
ments in chain saw design have dramatically reduced
the incidence.

The pathogenesis of the vibration syndrome is
unclear but has been shown to correlate with the du-
ration of exposure and the physical character of the
vibration: different frequencies and amplitudes pre-
dispose either to the osteoarticular lesions or to neu-
rovascular manifestations.^^' The effects of exposure
to vibrations are also influenced by ergonomic factors,
eg, how the tool is handled, and biological suscep-
tibility. Since vibration syndrome seems to pref-
erentially involve the ulnar artery, as does the HHS,
i it is not clear in the present case study which source
of trauma was more causative of the hand ischemia.

HHS and vibration syndrome are uncommon but
important causes of Raynaud's phenomenon. Both
syndromes are usually reversible if treated early and
appropriately. Diagnosis is important for proper treat-
ment, vocational counseling, and initiating disability
claims. Although known for many years, these syn-
■ dromes have not received wide publication in Amer-
ican medical literature and may be more prevalent
than commonly realized. ■

REFERENCES

1. Machleder HL: Vascular Disorders of the Upper Extremity. Mount Kisco,
New York, Futura Publishing Co, Inc, 1983.

2. Behrens V, Wasserman D, Carlson W, et al; Vibration syndrome in
chipping and grinding workers. / Occup Med 1984;26:765-788.

3. Conn J Jr., Bergan JJ, BeU JC: Hypothenar hammer syndrome: Post-
traumatic digital ischemia. Surgery i970;68:1122-1128.

4. Pineda CJ, Weisman MH, Bookstein JJ, et al: Hypothenar hammer syn-
drome: Form of reversible Raynaud's phenomenon. Amer } Med
1985;79:561-570.

5. Vayssairat M, Debure C, Cormier J, et al: Hypothenar hammer syn-
drome: Seventeen cases with long term foUow up. J Vase Surg 1987;5:838-
843.

6. Wasserman DE: Raynaud's phenomenon as it relates to hand-tool vi-
bration in the workplace. Am bid Hyg Assoc J 1985;46:10-14.

7. Little JM, Ferguson DA: The incidence of the hypothenar hammer syn-
drome. Arch Surg 1972;105:684-685.

8. Calenoff L: Angiography of the hand: Guidelines for interpretation. Ra-
diology 1972;102:331-335.

9. Coleman SS, Anson BJ: Arterial patterns in the hand based upon a study
of 650 specimens. Surg Gynec Obstet 1961;113:409-424.

10. Benedict KT, Chang W, McCready FJ: The hypothenar hammer syn-
drome. Radiology 1974;111:57-60.

11. Taylor W, Wasserman D, Behrens V, et al: Effect of the air hammer on
the hands of stonecutters. The limestone quarries of Bedford, Indiana,
revisited. Brit J bit Med 1984;41:289-295.

12. Bovenzi M, Petronio L, DiMarino F: Epidemiological survey of shipyard
workers exposed to hand-arm vibration. Int Arch Occup Environ Health
1980;46:251-266.

13. Miyashita K, Shiomi S, Itoh N, et al: Epidemiological study of vibration
syndrome in response to total hand-tool operating time. Br } Ind Med
1983;40:92-98.

14. Starck J: FEgh impulse acceleration levels in hand-held vibrating tools.
An additional factor to the hazards associated with the hand-arm vibra-
tion syndrome. Scand J Worl Environ Health 1984;10:171-178.

15. Lee EH, Evans JG: Vibration-induced white finger disease: a case report.
Can J Surg 1984;27:513-514.

Drs. Jones and Frusha are clinical assistant professors in the Dept of
Surgery at LSU School of Medicine in Baton Rouge.

Dr. Schellack is a clinical instructor in the Dept of Surgery at LSU

School of Medicine in Baton Rouge.

All three authors are also engaged in group private practice limited to

vascular surgery in Baton Rouge.

Reprint requests should be sent to Terry R. Jones, MD,
5329 Didesse Dr, Baton Rouge, LA 70808; (504)769-4493.

JOURNAL VOL 140 JANUARY 31

Physicians Recognition Award

Twenty-six physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
October, 1987. This award is presented by the American Medical Association to physicians who have voluntarily
completed 1 50 hours of continuing medical education during a consecutive three-year time period. Of these 1 50
hours, at least 60 must be in AMA/PRA Category 1. These twenty-six individuals are presented below.

Baton Rouge

Metairie

Frank Maurer Buckingham, MD
Richard Hugh Gold, MD
Gregory Orlando Harrison MD*

Charles Joseph Cucchiara, Jr., MD
Michael D. Horowitz, MD*

Chalmette

Michael Sydney Ellis, MD

Monroe

Felix Jefferson Willey, MD

Jennings

Scott Blume Gremillion, MD

New Iberia

David E. Bourgeois, MD

Kenner

Khalil Yousef Imsais, MD

New Orleans

Philip V. Beilina, Jr., MD
Theodore Joseph Borgman, MD
Robert McMurtry Gilliland, III, MD

Lafayette

Joan S. Grode Milner, MD
P. Safari-Kermanshahi, MD

Ernest Joseph Kaminski, MD
Abner Martin Landry, Jr., MD
Gordon Lee Love, MD*

Lake Charles

Thomas Paul Alderson, MD

David Anthony Newsome, MD*
Carlos Alberto Trujillo, MD
Robert Franklin Wood, MD

Marksville

Fernando Garcia Garcia, MD

Ruston

Nur Badshah, MD*

Marrero

Martin James O'Neill, Jr., MD

Winnsboro

Elvin Gregory Tubre, MD

* These individuals are not members of the Louisiana State Medical Society

32 JOURNAL VOL 140 JANUARY

A CASE OF METASTATIC CARCINOMA
IN ASSOCIATION WITH
PAGET’S DISEASE OF BONE

DAVID J. HOLCOMBE, MD

A previously healthy, 65-year-old black man was
diagnosed as having wide spread Paget's disease of
bone with a large lytic lesion in the right femur.
Curettage with prophylactic insertion of a rod was
performed and the surgical specimen tentatively
identified as sarcoma. Subsequent computed
tomography scan of the abdomen identified a left
suprarenal mass which was determined, from
percutaneous biopsy, to be a spindle cell renal
carcinoma similar histologically to the lytic lesion
in the right femur. Any uncertainty as to the
sarcomatous nature of tumors arising in pagetic
bone should evoke the possibility of carconima of

metastatic origin.

S PORADIC REPORTS of the association between met-
astatic carcinoma and Paget's disease of the bone
have been published. This rare association has been
attributed to the predilection of pagetic bone to met-
astatic seeding due to hypervascularization. ^ In all of
these previous cases, the confirmation of metastatic
carcinoma was made with biopsy. Unfortunately, the
histological picture may not always be clear-cut. Since
sarcomatous degeneration has been reported to occur
in 27% of patients older than 40 suffering from Paget's
disease,^ the diagnosis of osteosarcoma in the pres-
ence of a lytic lesion seems the most likely one^ in the
absence of any other observed tumor. Given the his-
tological variation in sarcomas,^ the possibility of met-
astatic carcinoma must, however, be considered when
the pathological findings appear sufficiently atypical.
In the case presented here, an initial tentative diag-
nosis of sarcoma was later modified to metastatic car-
cinoma when the presumed primary was located.

A 65-year-old black man with no significant past
medical history came to the emergency room three
times in one month with a chief complaint of right
thigh pain. He claimed to have been well until five
years prior to admission when he began having slight,

JOURNAL VOL 140 JANUARY 37

Fig 1 . Radiograph of pelvis and proximal femur re-
vealing extensive pagetic changes as well
as lytic lesion of right proximal femur.

intermittent, right upper thigh discomfort. During the
preceding month, the pain had grown progressively
worse and now was a dull ache, exacerbated by weight
bearing as well as by pushing on the brake pedal of
his car. The pain was slightly relieved by rest and did
not waken him from sleep. He denied any fever, chills,
anorexia, or weight loss. He had been treated symp-
tomatically with indomethacin, which had alleviated
the pain but did not eliminate it. At his last emergency
room visit, x-rays of the right hip and femur were
performed and revealed marked cortical thickening
of both bones compatible with Paget's disease and,
in addition, a large lucency in the proximal femur
eroding the cortex (Fig 1).

The patient had no allergies and was taking only

38 JOURNAL VOL 140 JANUARY

indomethacin (25 mg tid) as prescribed on a previous
emergency room visit. He was a retired truck driver,
now working as a school bus driver. He had smoked
one pack per day for 15 years and had drunk six cans
of beer a day for 10 years. Family history and review
of systems were noncontributory. The patient's blood
pressure was 120/80, his heart rate 80/min, and his
temperature 97° F. Physical examination was remark-
able only for pain on compression of the upper right
femur and for some fine disseminated inspiratory and
expiratory crackles in both lung fields. Laboratory ex-
aminations were remarkable for a normochromic,
normocytic anemia (hemoglobin 8.9 g/dL and he-
matocrit 27%), a platelet count of 566,000, an elevated
alkaline phosphatase of 205 U/L, and a sedimentation
rate of 62 mm/h. Urinalysis was negative. Later, a 24-
hour hydroxproline urinary excretion test proved to
be elevated at 110 mg/24 h. Chest x-rays showed
chronic lung disease with diffuse interstitial fibrosis
and focal fibrosis of the right perihilar region, and
focal fibrosis or infiltrate of the right perihilar region.
The ECG on admission was normal.

Subsequent bone scan and skeletal survey re-
vealed the presence of wide-spread pagetic involve-
ment of the right femur, right hip, left femur, right
tibia, both humeri, several vertebrae, and a right rib
posteriorly. The patient underwent surgical curettage
of the lytic lesion of the right femur and insertion of
a metallic intramedually rod as prophylaxis against
pathological fracture. The surgical specimen was ex-
amined and reported to be consistent with sarcoma,
with some reservation as to its exact characteristics
due to the absence of osteoid bone (Fig 2).

In order to exclude the presence of lung metas-
tases from the presumed sarcoma, not evident on the
routine chest films, the patient was sent for a com-
puted tomography CT scan of the lung which showed
a possible left upper lobe infiltrate as well as the pos-
sibility of very small bilateral effusions. At that time,
an abdominal CT scan was included because of the
suggestion of a left adrenal tumor. This CT scan dem-
onstrated the presence of nonenhancing left supra-
renal and right renal masses, previously unsuspected.
The left suprarenal mass underwent percutaneous bi-
opsy with a tentative diagnosis of carcinoma, prob-
ably renal, with spindle cell characteristics similar to
those previously identified as fibrosarcoma in the lytic
lesion of the right femur (Fig 3). The diagnosis was

Fig 2. Photomicrograph of bone biopsy from right
proximal femur, initially diagnosed as sar-
coma.

thus retrospectively transformed from one of sarcoma
arising out of pagetic bone to one of metastatic seed-
ing of carcinoma into pagetic bone.

The patient underwent radiotherapy to the right
femur with excellent symptomatic relief. Unfortu-
nately, he was readmitted two and a half months after
his initial hospitalization with complaints of increas-
ing weakness and shortness of breath. He died shortly
afterwards; subsequent autopsy confirmed the pres-
ence of a large hypernephroma of the right kidney
with a metastatic lesion in the contralateral adrenal
gland. In addition, disseminated metastatic lesions
were identified in both striated and cardiac muscle,
partially explaining his global weakness, dyspnea, and
late cardiac conduction problems. These widespread
metastatic lesions were uniformly less than 1 cm in
diameter, most of them being considerably smaller.

This case represents one of six reported in the
literature of metastatic carcinoma associated with Pa-
get's disease of bone. The possibility of such a diag-
nosis should be kept in mind, especially if the his-
tological diagnosis of presumed osteosarcoma appears
at all uncertain. ■

REFERENCES

1. Castleman B and McNeill M: Case records of the Massachusetts General
Hospital; weekly clinicopathological exercise 42292. N Engl } Med
1956;255:145.

Fig 3. Photomicrograph of suprarenal percuta-
neous biopsy specimen consistent with
carcinoma of kidney.

2. Agha FP, Norman A, Hirschl S, et al: Paget's disease. Coexistence with
metastatic carcinoma. NY State J Med 1976;76:734-735.

3. Kahnowski DT, Goodwin CA: Case Report 179: Metastic disease devel-
oping in Paget disease of bone in the distal end of femur. Skeletal Radiol
1981;7:229-231.

4. Hermann G, Szpom A, Schwarts I, et al: Metastatic carcinoma involving
Paget disease of the bone: An unusual association. Mt Sinai ] Med
1983;50(6):537-539.

5. Powell N: Metastatic carcinoma in association with Paget's disease of
bone. Br J Radiol 1983;56:582-585.

6. Huvos AG, Butler A, Bretsky SS: Osteogenic sarcoma associated with
Paget's disease of the bone. Cancer 1983;52:1489-1495.

7. Smith J, Botet JF, Yeh SDJ: Bone sarcomas in Paget's disease: A study of
85 patients. Radiology 1984;152:583-590.

ACKNOWLEDGMENTS

I would Hke to acknowledge the helpful assistance of
Miss Denise Ardoin in preparation of this manuscript.

Dr. Holcombe is an internist affiliated with Freedman Clinic of Internal

Medicine in Alexandria.

Reprints will not be available.

JOURNAL VOL 140 JANUARY 39

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child’s treatment can he a difficult decision for any
physician. At River Oaks, our staff understands the
special needs of both the patient and the family in
coping with mental illness, behavior problems, and
ennitional disorders. River Oaks — a private,
126 'hed facility, offers a broad range of programs for
the individual.

Long Term Care
Appropriate Medication
Crisis Center
Expressive Arts
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information on clinical

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admission or referral, contact the Admissions
Department, call us collect at (504) 734-1740;
Crisis Center, call 733-CARE; Outpatient Clinic
733-5591.

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RIVER OAKS PSYCHIATRIC CENTER

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(504) 734-1740

THE NEW ORLEANS CENTER FOR PSYCHOTHERAPEUTIC MEDICINE

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A Universal Health Services Facility

A COMMUNITY MEDICINE PROGRAM
IN JAMAICA FOR FOURTH YEAR
MEDICAL STUDENTS

IRWIN COHEN, MD

For two years, the Program in Community
Medicine of the Tulane University School of
Medicine has been sending fourth year medical
students to serve six to eight weeks continuous
rotations in rural health enters in Cornwall
County, Jamaica. Forty-nine students have gone
and 38 are scheduled for this year. The students
live in private homes and, assuming the duties of
a physician, become integrated members of rural,
district health care teams. The objectives of the
program are to 1) nurture humanism, 2) improve
history taking and physical examination skills, 3)
promote interest in primary health care,
community medicine, and the health team
approach to medical services, 4) supplement health
manpower in Jamaica, 5) develop interest in
developing-country work, and 6) develop a
universal perspective of life in the young
physician. Because the program is the result of an
agreement between a U.S. medical school and a
foreign government, is prearranged for the
student, and provides for a continuous student
presence at the foreign sites, it may well be a
unique feature of Tulane's medical curriculum.

T here are very few, if any, medical school-based
programs which regularly provide for a develop-
ing-country clerkship for undergraduate medical stu-
dents.^ There is no U.S. literature, except for personal
testimonies, documenting the effect of these experi-
ences on physicains and medical students.^ I believe
the effects can be multiple and salutary.

Two-thirds of the American public now believe
that people are beginning to lose faith in doctors.^
Patients assume that their physician is competent, but
they also strongly desire integrity, warmth, compas-
sion, attentiveness, effective communication, and en-
couragement from their physicians. These qualities
and skills are rarely nurtured in the science-laden un-
dergraduate medical curriculum. It is our belief that
medical students will recognize the role of humanism
in medicine if they are placed in a setting where there
is a dearth of modern medical support facilities, where
they will live where they work, and where they will
view their patients against the background of their
homes and communities. Hopefully, these experi-
ences will be remembered and will be used after they
return to improve patient relationships and the public
image of physicians.

JOURNAL VOL 140 JANUARY 41

Reductions in the cost of heath care
can be accomplished slowly by modi-
fying medical curricula and de-empha-
sizing expensive technology. The proc-
ess can be accelerated, however, by
immersing medical students in resource-
poor environments where they will dis-
cover that good patient histories and
careful examinations are their most pow-
erful diagnostic tools.

Medical education in the United States empha-
sizes scientific procedures and state-of-the-art tech-
nology. Impressive twentieth century advances in the
ability to manipulate biological systems foster phy-
sician dependence on expensive laboratory proce-
dures and curative medicine. However, health care
now consumes about 10% of the gross national prod-
uct; 40% of this health care share is publicly funded.
Physicians, because they control about 70% of na-
tional health spending, are being asked to develop
more cost-effective methods of patient management.^
Reductions in the cost of health care can be accom-
plished slowly by modifying medical curricula and
de-emphasizing expensive technology. The process
can be accelerated, however, by immersing medical
students in resource-poor environments where they
will discover that good patient histories and careful
examinations are their most powerful diagnostic tools.
This approach, when applied later in their medical
practices, can lead to a reduction in the total cost of
health care.

As public health care funds diminish, the im-
portance of using them efficiently increases. The
amount apportioned for the primary care of patients
will compete with that used for community health
problems. By fusing primary health care with com-
munity medicine and by rendering the service through
physician-led health teams, a broader view of soci-
ety's needs can be achieved. Although the decisions
will not be easier, they will be more accurate.^ Such
a dual focus is characteristic of the system in many
developing countries.^ A combined approach, stress-
ing both community health promotion and current
technology, is long overdue in this country. Ironi-
cally, the United States can look to developing coun-
tries for new approaches to cost-effective health serv-
ices.

Jamaica has a small national budget, of which an
inadequate amount is apportioned to health care serv-
ices.^ The small numbers of health care personnel re-
flect this. Physicians are in extremely short supply,
and this problem is worsening. The United States has
an abundance of physicians. Many are unaware of
overseas health care problems. Surely, we can (and
it is possible to mount a moral argument that we
should) encourage our physicians, perhaps either early
or late in their careers, to provide service to the people
of these nations.® This type of program will provide

42 JOURNAL VOL 140 JANUARY

some immediate relief to the people of Jamaica.

Opportunities to experience other health care
systems should be offered by all medical schools, al-
lowing nascent physicians to make more valid judg-
ments about components of their own system. And
in this instance, because Jamaica is resource-poor, be-
cause it has a decentralized and integrated primary
care and community medicine system, and because
it renders service through health care teams, under-
graduate medical students can gain valuable insights
about the humanistic and cost-control aspects of med-
icine.

Therefore, this program is an attempt to: 1) nu-
ture in young physicians feelings of humanism and
respect for the patient's dignity, 2) improve history
taking and physical examination skills in a resource-
poor setting to promote cost-effective health care, 3)
promote interest in primary health care, community
medicine and the health team approach to medical
services, 4) supplement manpower-poor health care
services in Jamaica, 5) stimulate interest in develop-
ing-country medical work, and 6) develop in the nas-
cent physician a universal perspective of life so nec-
essary to an educated person.

PROGRAM DESIGN

Fourth year medical students from Tulane University
and other U.S. medical schools elect to spend from
six to eight weeks living and working in Jamaica. They
live with Jamaican families in rural areas and are at-
tached to rural health care teams. Seven groups of
five students are successively and continuously sent
to the island.

Before departure, the students receive a brief ori-
entation to Jamaica, a Jamaica manual containing in-
formation collated from reports concerning island life
submitted by past students, and a commercially pro-
duced guide to Jamaica. After arrival, they are ori-
ented by the supervising Jamaican staff in Montego
Bay. The students then are transported to their rural
sites.

The sites, unfortunately, vary from session to ses-
sion depending on the availability of private home
accommodations. The sites used thus far are Fal-
mouth, Adelphi, Cambridge, Maroon Town, Hope-
well, Sandy Bay, and Lucea, all on the western end
of the island in the parishes of Trelawny, St. James
and Hanover.

Duties are determined by the activities of the dis-
trict health care teams and the parish health depart-
ments. They include medical, pediatric, obstetric and
gynecologic clinics at large and small outreach facil-
ities, home visits, lectures to primary and secondary
schools, churches and health-oriented community
groups, and visits to private and public commercial
facilities with public health inspectors. They provide
service to a clinic treating sexually transmitted dis-
eases, an old age home, and an orphanage in Montego
Bay. The students can arrange to spend time in the
Casualty Department or on in-patient services at
Cornwall Regional Hospital.

They are required to spend one week in Kingston
with the Department of Social and Preventive Med-
icine at the University of the West Indies. They live
in the homes of professors, visit the outreach facilities
of this large, metropolitan area and take classes with
and meet Jamaican medical students.

They are also required to formulate and conduct
an epidemiologic project. The data are organized into
a written report and are presented at an end-of-the-
year seminar. The studies are then combined in the
form of a report to the Cornwall County Public Health
Department.

The entire cost of the trip ($800 to $1000) is borne
by the student. Humanitarian discounts for air travel
have been generously granted by Eastern and Air
Jamaica Airlines.

RESULTS

During the first two years, 49 students (43 from Tu-
lane Medical School) and three residents (from pe-
diatric and family practice residencies) worked in Ja-
maica. This year 38 students are scheduled (34 from
Tulane). The latter group of students is not discussed
in this report.

Twenty-six of the Tulane medical students were
men. This reflects exactly the percentage of men in
this year's graduating class. The students averaged
2.0 high passes per person (Tulane's highest grade)
in their third year clinical clerkships. The entire grad-
uating class averaged 1.9 per person. Eighteen stu-
dents planned to do residencies in internal medicine,
nine in surgery, six in pediatrics, and six in obstetrics
and gynecology. Only two planned to enter family
practice residencies. Except for surgery, a greater per-
centage of this group is entering graduate training in

JOURNAL VOL 140 JANUARY 43

each of the above disciplines when compared to the
entire graduating class. Nine students planned to
practice general internal medicine, six some form of
surgery, six pediatrics, and six obstetrics and gyne-
cology. Only one student indicated a preference for
each of family practice, public health, and third world
medicine. Twenty-three students indicated they were
going to establish a private practice while 18 were
planning to enter academia.

Before leaving, multiple reasons were usually
given by the students for wanting to take this elective.
Thirty-five students indicated that they wanted to ex-
perience Third World medicine. Thirteen felt the ex-
perience would improve their clinical skills in am-
bulatory medicine. Seven felt they wanted to make a
contribution to humanity and seven chose reasons of
convenience (cost, English is spoken, the trip was
organized).

After returning, each student listed multiple ben-
efits they derived from the program. Forty felt that
they improved their ambulatory clinical skills and were
more confident in using them. Six specifically men-
tioned how the unavailability of laboratory studies
enhanced this effect. Twenty-seven were impressed
by the cultural differences they experienced. Twenty-
six used the opportunity to compare our medical care
system with that in Jamaica. Fourteen appreciated the
increased independence and responsibility they were
given and six felt they became better-educated per-
sons.

In assessing the program, 18 used the word “ex-
cellent"; others called the program "fantastic," "mag-
nificent," "extremely valuable"; one student felt this
"was the best cUnical course" she took and two wanted
to go again.

On the other hand, seven students felt the need
for better on-site supervision and orientation sessions
and three felt that a laboratory and library at the rural
sites were essential.

I have had two conferences with Jamaican health
care workers about student performance. Praise of
their medical knowledge and enthusiasm was uni-
versal. Everyone thought that the program should
continue.

DISCUSSION

Jamaica was chosen as the country for this student
program for the following reasons: it is close to the

44 JOURNAL VOL 140 JANUARY

United States mainland (making travel cheaper), it is |
a safe environment for expatriate health care workers, ^
the students can live in the community where they
work, English is the language, the people are in need,
there is an existing, but poorly-financed primary health
care community medicine infrastructure, there is an
established medical school, and I know many of the
people who organize health care delivery on the is-
land.

In answer to the few criticisms made by the stu-
dents and the Jamaican staff, the program will now
begin with an expanded one and one-half hour ori- ;
entation session at Tulane University. Field supervi-
sion and in-country orientation sessions will be pro-
vided by a Jamaican physician who will be hired by j
Tulane University. He will meet the students at the
airport, inform them of the nature of the Jamaican
health care system, medical personnel, local services,
available medicines, living conditions, the trip to
Kingston, the epidemiologic project, and how the stu-
dents may integrate with Jamaican rural health care ,
work and life. Libraries are being slowly created with
discarded medical texts by students. The availability
of laboratory services is the responsibility of the host
country. The recurring costs of such services preclude
their funding by this program. Furthermore, it is their
absence which makes Jamaica a desirable site.

The students who selected the program were a
reflection of the graduating class with regard to sex
and clinical grades distribution. A greater percentage
of the program group is entering the graduate training
programs of the primary care disciplines. This was
especially evident in medicine (29% versus 42%). As
a consequence, surgical training programs are un-
derrepresented in the Jamaica group (29% versus 21%).

It is tempting to believe that this elective, being an
ambulatory, general practice experience, can serve as
a marker for those students who wiU choose work in
a primary care, private practice setting. However, 42%
of this group also plans to enter academia.

This is a preliminary report. Whether this pro-
gram can achieve all its objectives is unknown. At
present, the students do help to alleviate Jamaica's
health care manpower shortages and Jamaican health
care workers have repeatedly told me of their effec-
tiveness.

The effect of the experience on the students is
only suggested by their comments. Almost all appre-

dated the opportunity to practice and refine their clin-
ical sldlls, and a few mentioned how the resource-
poor environment facilitated this objective. Whether
this appredation translates into less reliance on ex-
pensive technology as sldlls mature is unknown.

Perhaps because students Uved in private homes
in the communities where they worked and met and
studied with Jamaican medical students, most were
impressed by the cultural differences of our two so-
deties and by the differences in our health care de-
livery systems. The experiential nature of this knowl-
edge may strongly influence future activity in primary
health care, community medicine, or developing
country medical work. One student, after returing,
did state that he was now planning to work in de-
veloping countries, and five became more aware of
the health needs of the poor and how local access
solves one of those needs.

Sadly, no one specifically mentioned the human-
ism of the enterprise; the opportunity to see the effect
of illness and physician recommendations on patients
in their homes and communities. Only two students
reflected on their place in the world and on the char-
acteristics of a well-rounded person. Perhaps this is
because medical schools train doctors, they do not
educate them. The training leaves the neophyte only
with the knowledge that powerful curative medical
tools exist, but without a knowledge of how to use
them. Without exposure to the humanities, they are
left without a broad view of humanity and the uni-
verse and without a tempering kernel of humility. It
is, in part, humility which prompts us to accept the
reality of being a part of the inhumanity and human
tragedy which surrounds us, and yet not to forget
that with our special sldlls we can be powerful actors
in the struggle to bring about a particle of social jus-
tice. If medical curricula cannot include the human-
ities, then immerse the medical student in the world
— not in the hospital. There he wiU learn of the po-
tential the practice of medicine holds for continuous
professional satisfaction.

Student and staff feedback suggest that, in the
short run, the program is a success. Its potential value
in shaping desirable characteristics in developing
physicians can only be revealed by a prospective study
of the future professional activities of today's Jamaica
influenced students. ■

l\/l edical schools train doctors, they do
not educate them. The training leaves the
neophyte only with the knowledge that
powerful curative medical tools exist, but
without a knowledge of how to use them.
Without exposure to the humanities, they
are left without a broad view of human-
ity and the universe and without a tem-
pering kernel of humility. ... If med-
ical curricula cannot include the human-
ities, then immerse the medical student
in the world — not in the hospital.

ACKNOWLEDGMENTS

Without the diligent, voluntary efforts of Dr. Marjorie
Holding, Senior Medical Officer (Health), Cornwall
County; Dr. SheHa Campbell, Medical Officer (Health),
St. James Parish; and Dr. Denise Eldemire, Depart-
ment of Social and Preventive Medicine, University
of the West Indies, this program would not have been
possible.

REFERENCES

1. Baker TD, Quinlv JC: A U.S. International Health Service Corps. JAMA
1987;257:2622-2625.

2. Gorton MM: Hospital practice in Nepal. N Engl J Med 1985;312:249-250.

3. Mechanic D: Public perceptions of medicine. N Engl J Med 1985;312:181-
183.

4. Spivey BE: The relation between hospital management and medical staff
imder a prospective payment system. N Engl J Med 1984;310:984-986.

5. Nutting PA: Community oriented primar}' care: A promising innovation
in primary care. Public Health Rep 1985;100:3-4.

6. Second Population Project, Jamaica, 1976-1980. Ministry of Health and En-
vironmental Control, Government of Jamaica, 1976.

7. Pocketbook of Statistics. Jamaica, Statistical Institute of Jamaica, 1983.

8. Pust RE: U.S. abundance of physicians and international health. JAMA
1984;252:385-388.

Dr. Cohen is from the Program in Community Medicine at Tulane
University School of Medicine in New Orleans.

Reprints will not be available.

JOURNAL VOL 140 JANUARY 47

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48 JOURNAL VOL 140 JANUARY

JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY February 1988

Micromrgery 1987: The tSU experience

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JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY 1988

VOLUME 140 / NUMBER 2 / FEBRUARY

ARTICLES

Blood pressure control
in children

James W. Wade, MD
Roy F. Brabham, MD
L. Franklyn Elliott, MD

Microsurgery 1987:
The LSU experience

Krishna Gravois, MD

Sonographic evaluation
of acute bacterial

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Bruce A. Baethge, MD
Robert E. Wolf, MD, PhD

Gold-induced

pneumonitis

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|)(()Vidc i)hi( li< ,il s( icfili(i< infortii.ilioii of iMicrcsl lo <i brf^.id s|)(‘( triim
of |)liysi( I. Ill iiicmlicrs of the I SMS <iiid lo incct ific ii(‘cd of c,k li ptiysi-
( l.iii lo iii.iinl.iin .1 f^i'iicr.il .iw.ircncss of progress <ind ( Ii.iiiko in < linii <il
iiicdii iiic, I lie ( onicnl is dcsi^iiofl lo .lid llic pr.K lit ing |)hysi( i.iii in
giving ( oniprcimisivc < <irc rind in rc< ogni/ing llic nood for s|)C( i,il-
i/cd li(’.ilnicnl,

llic lOUKNAi, welcomes iiMleri.il for public .ilion if submilled by <i
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TITl.E PACiE should c <iriy 1 1 1 llic* lillc* of llic* m.inusc ripl, wliic li should
be* c one isc* bul iniorni.ilivc*; |21 full ii.inic* of c*,u li .lullior, wilb liiglic'sl
.1C .iclc*niic clc*grc*e*(s), lisic'cl in clc*sc c*ncling orclc*r of m.igiiilucic* of c cin-
Iribiilion (only llic* n.imc's of lliosc* who li.ive* c oiilribulc*d ni.ilc*ri.illy
lo llic* prc*p.ii. Ilion of llic* m.inusc ripl should be* inc luclc*cl); | f| ,i onc*-
lo lwo-sc*nlc*nc c* biogr.i|)liic <il clc*sc lijilion for c*.ic li .lullioi wliic li should
inc luclc* spc*c i.illy, pi.ic lie c* loc .ilion, .ic .iclc*niic <ippoinlnic*nls, prim.iry
lios|)il.il .iliili. Ilion, or ollic*r c rc*clils (.i pic lure*, bl.ic k-.ind-wliilc* lic*.icl
sliol, of c*.ic 11 .lullioi ni.iy <ilso be* sc*iil if .iv.iil.ibic*); |4| n.imc* .ind .icl-
clic*ss ol .lullior lo whom rc*c|uc*sls for rc'prinis should be* .iclclrc*ssecl,
or .1 sl,ilc*nie*nl ih.il rc*priiils will nol be* .iv.iil.ibic*.

ABSTRACT should be* on llic* sc*c oiicl ji.igc* .ind c onsisi of no more* ih.in
ISO words. Il is clc*sigiic'd lo .icciu.iini ihc* polc*nli.il rc*.idc*r wilh ihc*
i*ssc*nc c* of ihc* lc*xl .iiicl should be* inform.ilivc* r.ilhc*r ih.in desc riplivc*.
(Avoid lc*lling wh.il "will be* cic'sc ribc*cl" .ind insic'.icl clc*sc ribc* il.) The*
.ibsir.ic I should be* inlc*lligiblc* whc*n divorc c*c! from ihc* .irlic Ic*, clc*voicl
ol unclc*finc*cl .ibbrc*vi. ilions, .iiicl suil.ibic*, willioul rc*wriling, for
rc*produc lion by .ibsir.ie ling sc*rvic c*s. I he* .ilisir.u I should c onl.iiii: 1 1 1
.1 briel sl.ilc*mc*nl ol ihc* m.inusc rijil's purpose*; (2| ihc* .ijipro.ic h usc'cl;

I l| ihc* m.ilc'ii.il sluclic*cl; |4| llic* rc*sulls c)bl.iinc*cl. I iiiph.isi/c* iic'w .ind
impoil.iiil ,ispc*c Is oi ihc* slucly or obsei'v.ilions.

KEY WORDS sfiould follow ihe .ibslrncl .ind be* idc*ntified as such.
I'rovidc* lhrc*c* lo five* kc*y words or short jihr.isc's that will assist index-
c*rs in c ross-indc*xing your .irlic Ic*. Use* lc*rms from the Medic al Sub-
jc*cl llc*.iding list from lnclc*x Mc*dicus when jiossifile.

SUBHEADS .irc* strongly c*iic ouragc*d. They should jirovidc* guidanc e
for ihc* rc*.iclc*r .me) s(*rvc* lo fire.ik the* tyjiograjihic monotony of the
lc*xl. Ihc* formal is flc*xiblc* but subheads cirdinarily inc lude*: Methods
.md M.ilc*ri.ils, C.isc* Kc*j)orls, Synijiloms, Examination, Trc*alment and
lc*( hnic)uc*, Kc*sulls, Discussion, and Summary.

REEERENCES must fic* cloublc*-st).ic c*cJ on a s(*j)arate shc*et of jiajic'r and
limilc*d lo .1 rc*.ison.i/i/c* numbc*r. Tlic*y will fie critically examinc*ci al
llic* lime* of rc*vic*w .md must fic* kejil to a minimum. All references
must lie* c ilc*cl in ihc* lc*xl and ihc* list should fic* arrangc*cl in order of
c il.ilion, nol alpli.ific*tic .illy. Pc*rscin.il ccimmunic ations and unpufilishc‘d
cl.il.i sfiould nol fic* inc luc)c*d in rc*fc*rc*nces, but shoulcf fic* inc orporalc^d
in ihc* lc*xl. flic* following form sfiould lie* fcillciwc*d:

lOUKNAl.S

1 1 1 Author(s): Use* the* surname* fcillowe*d liy initials without jiunctua-
lion, flic* ii.ime*s of .ill .lulhors should fic* give*n unless there are more
than lhrc*c*, in which case* the* name's of the first thre*e* authors are
usc*d, followc'd by "e*l al." |2) Title of article. Cajiitali/e only the first
lc*tte*r of Ihc* first word. ( f) Name of journal FollowecJ by no punctua-
tion, unclc*rsc orc*cl, and alilirc*vi.ilc*d acccirding to Index Mc'dicus. (4)
Year of publication; |.5| Volume number: Do not include* issue number
or month e*xc e*pl in the* c ase* of a su|ijile*me*nl or when jiaginaticin is
nol c onse*c ulivc* ifiroughoul tfie volume*. |6| Inclusive page numbers.
Do nol omil digits.

Ex.implc*: Itor.i 1 1, l).iiiiic*m 1 1, St.inforcl W, c*t .il: A guiclc*line fcir lilocicl

use* during surgc*ry. Am I (Jin I^Jlhol 1979;71:680-692.

HOOKS

1 1 1 Author(s): Use* the* surname* follciwc*d fiy initials without jiunctua-
lion. Ihc* n.mic*s of .ill .uithors should lie* given unle*ss the*re are more
Ih.in lhrc*e*, in wliic h c .ise* the* name's of the* first three authors are used
fcillowc'cl by "c*l .il." 12 1 Title, Cajiitalize the first and last word and
c'.ic h word ih.il is nol an .irlic le, |ire*(icisiticin, or conjunction of less
Ih.m four lc*llc*rs. | f| Edition number, |41 Editor's name. |5] Place of
publication, (hi Publisher, (71 Year, (H] Inclusive page numbers. Do
not omit digits.

Ex.impk‘: l)c*(iolc* (I , Spann E, I lursi KA |r, c*l al; Hodsido Examina-

tion in ( ardinvasc iilar M('di( ino, c*cl 2, Smith |T (c*d). New
York, McC.r.iw Hill Co, 1986, pj) 2J-J7.

ILLUSTRATIONS should fic* submiltc'd in duplicate in an envelope*
(p.ijic'r c lijis should nol lie* use*cl on illustrations since the indentation
lhe*y make* may show on re'produc ticin). Legends should fie typc'd,
cloublc*-spac c*d on .i sc'par.ilc* shcH'l of |ia|ier. Pholograjihic material
should be* high-c onirast glossy jirints. Patients must be unreccignizafile
in phc)lcigra|ihs unless spe*c ific wrille*n conse'nt has bc*e*n ofitainc'd, in
whic h c .ise* .i c eijiy of the* authori/alion should ac c cimjiany the
m.inusc rijit. Omit illtiJraliotts witich do not increase understanding
ol text. Illusir.ilions must fie* limite*cl lo a reasonalile number (four il-
luslr.ilions should be* .idc'ciu.ilc* for a manuscrijil of 4 to 5 tyjie'd pages).
Ihc* following inlormalion should fie ty|ie*cl on a lalic'l and affixc'd to
the* li.u k of e*ac h illusir.ilion: figure numbc*r, title of manusc rijit, name
of se'iiior .uilhor, .ind arrow indicating top.

TABLES should be* se'lf-ex|ilanatory and should sujiplement, not
duplicate*, the* le*xl. E.u h should be* tyjic’d on a sejiarate* shee't of pajier,
numbe*rc'cl, .md have* a brie'f de*sc rijitive title.

ACKNOWLEDGMENTS are* Ihe* author's jirerogative; howewer,
ac knowle'dgmeni ol lec hnic i.ins and other remuneratc'd jiersonnel for
c .irrying oul routine' c)|ier.ilicins, or of resident physicians who merely
c .ire* for |i.ilic*nls .is jiarl of ihc'ir hosjiital clutie's is discouragc'd. More
,ic c c'pl.ible* .K kiiowlc'clgme'iils inc lude those of intellectual or profes-
sional jiartic i|i.iticin.

GALLEY PROOES will be* maile'd to the jirincitial author for corre’c-
lioiis. kepriiil ordc'rs forms will accompany galle*y jiroofs.

NEW MEMBERS

Applications for membership have been re-
ceived from the following physicians by the
respective parish medical societies as of De-
cember 8, 1987. The Louisiana State Medical
Society is pleased to welcome:

■ East Baton Rouge

William A. Anderson III, MD

5412 Dijon Dr, Baton Rouge 70808

1982, LSU School of Medicine, New Orleans
internal medicine

Gerald M. Barber, MD

4609 North Blvd, Baton Rouge 70806
1984, LSU School of Medicine, New Orleans
family practice

Jeffrey G. Breaux, MD

6300 Main St, Bldg G, Suite A, Zachary 70791

1983, Tulane University School of Medicine
obstetrics & gynecology

N. Joseph Deumite, MD

5228 Dijon Dr, Baton Rouge 70809
1980, LSU School of Medicine, New Orleans
internal medicine

George W. Evans, MD
3600 Florida Blvd, Baton Rouge 70806
1954, University of Pennsylvania School of
Medicine
pathology

Robert S. Fields, MD

4950 Essen Lane, Baton Rouge 70809
1975, Jefferson Medical College, Philadel-
phia

radiation oncology

Milton G. Fort, MD

5825 Airline, Baton Rouge 70805
1977, Baylor College of Medicine
obstetrics & gynecology

Nancy N. Grinton, MD
8212 Summa Ave, Suite B, Baton Rouge
70809

1979, LSU School of Medicine, New Orleans
anesthesiology

Richard D. Hanson, MD

5422 Dijon, Baton Rouge 70808

1982, LSU School of Medicine, New Orleans

diagnostic radiology

Roberta J. Hawk, MD

1401 North Foster Dr, Baton Rouge 70806

1982, Tulane University School of Medicine
dermatology

Francis H. Henderson, MD
673 East Airport Ave, Baton Rouge 70806
1962, Howard University School of Medi-
cine, Washington, DC
obstetrics & gynecology

Daniel H. McNeill Jr, MD

2041 Silverside, Suite A, Baton Rouge 70808

1973, University of North Carolina School
of Medicine

diagnostic radiology

Beverly W. Ogden, MD

1516 Jefferson Hwy, New Orleans 70121

1983, Tulane University School of Medicine
pathology

Glen J. Schwartzberg, MD
7525 Picardy Ave, Suite C, Baton Rouge
70809

1980, Tulane University School of Medicine
vascular surgery

Mark C. Shoptaugh, MD

8212 Summa Ave, Suite B, Baton Rouge
70809

1984, LSU School of Medicine, New Orleans
anesthesiology

Sterling E. Sightler, MD

7662 Goodwood Blvd, Suite B201, Baton
Rouge 70806

1982, LSU School of Medicine, New Orleans
obstetrics & gynecology

■ Iberia

L. Barrow Bourgeois, MD
1409 Church St, Jeanerette 70544

1974, LSU School of Medicine, Shreveport
family practice

■ Jefferson

Grace A. Banuchi, MD
151 Meadowcrest St, Suite C, Gretna 70056
1976, University of Puerto Rico School of
Medicine
pediatrics

Mark Dal Corso, MD
3456 Jurgeus, Metairie 70002
1984, University de Monterrey Instituto
Ciencias de la Salud Facultad Medicina,
Mexico
pediatrics

Thiem Dang, MD

105-C Westbank Expressway, Gretna 70053

1972, Faculte Mixte de Medecine et de Phar-
macie University de Saigon, South Viet-
nam

family practice

Edmund K. Kerut, MD

4500 Wichers Dr, Marrero 70072
1982, University of Mississippi School of
Medicine
cardiology

John J. Knox, MD

PO Box 949, Civic Dr, Port Sulphur 70083

1973, University of Iowa College of Medi-
cine

internal medicine

Elenita S. Mata, MD

151 Meadowcrest St, Gretna 70056

1980, Institute of Medicine Far Eastern Uni-
versity, Philippines

pediatrics

Joseph H. Puente, MD

4315 Houma Blvd, Metairie 70002

1981, American University of the Caribbean
internal medicine

Richard R. Roniger, MD

4315 Houma Blvd, Metairie 70002

1968, LSU School of Medicine, New Orleans

psychiatry

■ Lafayette

Jack A. Hurst, MD

110 Hospital Dr, Lafayette 70503

1979, LSU School of Medicine, New Orleans

neurological surgery

Steven Jacobs, MD

4212 West Congress, Lafayette 70503

1982, University of California School of
Medicine, Los Angeles

ophthalmology ^

JOURNAL VOL 140 FEBRUARY 3

Earl Washington Jr, MD

850 North Pierce St, Lafayette 70501

1978, Tulane University School of Medicine
gastroenterology

M Rapides

Vernon W. Cantwell, MD

PO Box 669, Olla 71465
1986, University of Texas Medical School,
San Antonio
general practice

Dave M. Rayburn, MD

390 Griffith St, Pineville 71360

1982, LSU School of Medicine, Shreveport
general surgery

■ River Parishes

Vern E. Meyer, MD

16A Storehouse Lane, Destrehan 70047
1974, Medical College of Virginia Common-
wealth University School of Medicine
pediatrics

■ Shreveport

Motaz Albahra, MD

1850 Martin Dr #922, Bossier City 71111

1979, Faculty of Medicine University of
Aleppo, Syria

pathology

Bruce A. Baethge, MD

PO Box 33932, Dept of Internal Medicine,
Shreveport 71130

1978, University of Texas Southwestern
Medical School

internal medicine

Michael J. Cone, MD

8701 Creswell Rd, Shreveport 71104

1979, LSU School of Medicine, Shreveport
neonatal/ perinatal

Roan L. Flenniken, MD

8730 Youree Dr, Shreveport 71115

1983, LSU School of Medicine, Shreveport
internal medicine

Patrick T. Gallagher, MD

2510 Bert Kouns Industrial Loop, Shreve-
port 71129

1982, LSU School of Medicine, Shreveport
emergency medicine

B. Kishore Gupta, MD

PO Box 33932, Dept of Psychiatry, Shreve-
port 71130

1974, Kasturba Medical College, Mysore
University, India
psychiatry

William H. Haynie Jr, MD

1035 Creswell, Shreveport 71101

1982, LSU School of Medicine, Shreveport
internal medicine

Mark E. Janulewicz, MD

1035 Creswell, Shreveport 71101
1975, University of Nebraska College of
Medicine
family practice

Jacque T. LaBarre, MD

207 Winged Foot, Shreveport 71106

1983, LSU School of Medicine, Shreveport
obstetrics & gynecology

Judy D. Laviolette, MD

2532 Bert Kouns, Suite E107, Shreveport
71118

1984, LSU School of Medicine, Shreveport
internal medicine

Susan A. Lee, MD

2355 Bert Kouns, Suite E107, Shreveport
71118

1984, University of Texas Medical School,
San Antonio
family practice

Larry C. Moore, MD

1035 Creswell, Shreveport 71101

1980, University of Texas Medical Branch,
Galveston

cardiology

John M. Provenza, MD

2533 Bert Kouns, Suite 107, Shreveport 71118
1984, LSU School of Medicine, Shreveport
internal medicine

Hiram M. Vazquez, MD

1530 Line Ave, Shreveport 71104

1981, Universidad Nordestana, Dominican
Republic

anesthesiology

■ St. Tammany

Thomas J. Dewey III, MD

1045 Elorida Ave, Slidell 70458

1967, LSU School of Medicine, New Orleans

orthopedic surgery

Joseph A. Pedone, MD

1323 South Tyler, Covington 70458
1977, LSU School of Medicine, New Orleans
internal medicine

■ Tangipahoa

Brian C. Ball, MD

1003 Delural Blvd, Hammond 70403
1984, LSU School of Medicine, New Orleans
anesthesiology

■ Terrebonne

Conchita J. Lazarraga, MD
1978 Industrial Blvd, Houma 70363

1977, University of the East, Philippines
pediatrics

Ronald J. Long, MD

1978 Industrial Blvd, Houma 70363

1978, Indiana University School of Medicine
obstetrics & gynecology

Ursula S. Long, MD

1978 Industrial Blvd, Houma 70363

1978, Northwestern University Medical
School

anesthesiology

■ Intern/ Resident Members

CALCASIEU

Francine A. Manuel, MD

1000 Walters, Lake Charles 70601

1985, LSU School of Medicine, New Orleans ,

family practice i

■ Service Members

SHREVEPORT

Daniel J. Culkin, MD

PO Box 33932, Dept of Urology, Shreveport
71130

1979, Creighton University School of Med-
icine, Omaha

urology

4 JOURNAL VOL 140 FEBRUARY

TAX QUALIFIED RETIREMENT PLANS

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Dista Products Company

Diviston of Eli Lilly and Company
Indianapolis, Indiana 46285
Mfd by Eli Lilly industries, Inc
Carolina, Puerto Rico 00630

□ ISTA

Computer-generated molecu
structure of cephalexin
hydrochloride monohydrate

® 1987, DISTA PRODUCTS COMPANY KX-9008-B-849336

Convenient 500-mg b.i.d.
dosage and demonstrated
effectiveness for
treatment of:

□ skin and skin structure infections^^

□ uncomplicated cystitis^

□ pharyngitis*

• New hydrochloride salt form of cephalexin—
requires no conversion in the stomach before
absorption

• Well-tolerated therapy

• May be taken without regard to meals

^or other indicated infections, 250-mg tablets available
brq.i.d. dosage

=*riced less than Keflexlcephaiexin)

Keftab is contraindicated in patients with known allergy to the
cephalosporins and should be given cautiously to penicillin-
sensitive patients.

Penicillin is the drug of choice in the treatment and prevention
of streptococcal infections, including the prophylaxis
of rheumatic fever.

K 'Due to susceptible strains of Staphylococcus.aureus and/or /3-hemolytic streptococci.

Due to susceptible strains of Escherichia coli. Proteus mira'bilis. and Klebsiella sp.

If Due to susceptible strains of group A 0-hemolytic streptococci.

KEFTAB"

(cephalexin hydrochloride monohydrate)

Summary: Consult the package literature for
prescribing information.

Indications and Usage:

Respiratory tract infections caused by susceptible
strains of Streptococcus pneumoniae and group A
i3-hemolytic streptococci.

Skin and skin structure infections caused by sus-
ceptible strains of Staphylococcus aureus and/or
/3-hemolytic streptococci.

Bone infections caused by susceptible strains of
S aureus and/or Proteus mirabilis.

Genitourinary tract infections, including acute pros-
tatitis, caused by susceptible strains of Escherichia
coli, P mirabilis, and Klebsiella sp.

Contraindication: Known allergy to cephalosporins.

Precautions:

• Discontinue Keftab in the event of allergic reac-
tions to it.

• Prolonged use may result in overgrowth of nonsus-
ceptible organisms.

• Positive direct Coombs’ tests have been reported
during treatment with cephalosporins.

• Broad-spectrum antibiotics should be prescribed
with caution in individuals with a history of gas-
trointestinal disease, particularly colitis.

• Safety and effectiveness have not been determined
in pregnancy and lactation. Cephalexin is excreted
in mother’s milk. Exercise caution in prescribing
Keftab for these patients.

• Safety and effectiveness in children have not been
established.

Adverse Reactions:

• Gastrointestinal, including diarrhea and, rarely, nau-
sea and vomiting. Transient hepatitis and chole-
static Jaundice have been reported rarely.

• Hypersensitivity in the form of rash, urticaria, angio-
edema, and, rarely, erythema multiforme, Stevens-
Johnson syndrome, or toxic epidermal necrolysis.

• Anaphylaxis has been reported.

• Other reactions have included genital/anal pruri-
tus, genital moniliasis, vaginitis/vaginal discharge,
dizziness, fatigue, headache, eosinophilia, neutro-
penia, and thrombocytopenia: reversible interstitial
nephritis has been reported rarely.

•Cephalosporins have been implicated in trigger-
ing seizures, particularly in patients with renal
impairment.

• Abnormalities in laboratory test results included
slight elevations in aspartate aminotransferase
(AST, SCOT) and alanine aminotransferase (ALT,
SGPT). False-positive reactions for glucose in the
urine may occur with Benedict’s or Fehling's solu-
tion and Clinitest® tablets but not with Tes-Tape®
(Glucose Enzymatic Test Strip, USR Lilly).

PV 2060 DPP [091887] 849336

BLOOD PRESSURE CONTROL

IN CHILDREN

The following is reprinted by permission at the request of the Louisiana
State Medical Society Committee on Chronic Diseases. It is excerpted
from the National Heart, Lung, and Blood Institute's "Report of the
Second Task Force on Blood Pressure Control in Children - 1987" which
appeared in Pediatrics [1987;79(1);1-25],

All physicians who care for children 3 years of age through adolescence should be
encouraged to measure blood pressures (BPs) once a year, when the child is well. This
is because BP is a physiologic parameter, which when elevated becomes a risk factor,
either for the development of hypertension itself or for the development of premature
cardiovascular morbidity, if not during childhood, then during adulthood. BP measure-
ment should be included in the physical examination as part of the continuing care
of the child, not as an isolated procedure. BPs should also be measured in symptomatic
children, children in emergency rooms and intensive care units, and in high-risk in-
fants, because an elevated BP may complicate certain diseases or be a marker of future
hypertension. At the time of examination, the patient or parent should be told that the
BP is normal, high normal, or hypertensive and whether further surveillance is indicated.
It should be clearly stated that the finding of single modestly elevated reading does
not constitute a diagnosis of hypertension but does indicate the need for further evalua-
tion including repeated measurements over time. Children with severely elevated
readings should be evaluated immediately.

8 JOURNAL VOL 140 FEBRUARY

Norton W. Voorhies, MD, Editor

ECG OF THE MONTH

ELEGANT, BUT INCOMPLETE

JORGE I. MARTINEZ-LOPEZ, MD

The tracing shown below consists of seven leads from a 12-lead scalar ECG received at the Heart
Station without patient identification or information relative to the clinical diagnosis and treat-
ment.

What is your diagnosis? Elucidation is on page 13.

JOURNAL VOL 140 FEBRUARY 11

REPORTING AIDS CASES IN LOUISIANA

WHO SHOULD REPORT?

Every physician is required by law to report any case or suspected case of AIDS which he or she is attending,
has examined, or has prescribed for (Louisiana Sanitary Code, Chapter II, §2:004).

WHAT SHOULD BE REPORTED?

The presence of a reliably diagnosed disease at least moderately indicative of an underlying cellular immune
deficiency, with no other known underlying cause of cellular immune deficiency nor any other cause of reduced
resistance reported to be associated with that disease. This involves completion of a two-page case report
form (available from the Epidemiology Section or any parish health unit) to determine if the person meets
the Centers for Disease Control AIDS surveillance case definition.

WHEN SHOULD 1 REPORT?

The report should be made promptly at the time the physician first visits, examines or prescribes for the
patient (Louisiana Sanitary Code, Chapter II, §2:004).

WHERE SHOULD 1 REPORT?

A diagnosed or suspected case of AIDS should be reported directly to the Epidemiology Section in New
Orleans.

By phone: (504) 568-5005

By mail: La. Office of Preventative and Public Health Services
Epidemiology Section
PO Box 60630
Room 615

New Orleans, LA 70160

WHY REPORT AIDS CASES?

In addition to being required by law, monitoring the distribution and characteristics of patients with AIDS
is the only method currently available for detecting changes in the epidemiology of Human Immunodefi-
ciency Virus (HIV). Knowledge of the impact of HIV on Louisiana residents can help detect new or unusual
modes of transmission and assist in targeting high risk groups for education and prevention programs.

CONFIDENTIALITY CONCERNS

All reports are kept absolutely confidential. Names of patients, physicians or hospitals are not released under
any circumstances.

ECG of the Month

Case presentation is on page 11.

DIAGNOSIS — Atrial fibrillation with advanced AV block

Because of the total lack of information with respect
to the patient whose tracing is shown here, the dis-
cussion to follow starts with a description of the ECG

( findings and ends with comments on their possible
clinical significance.

DISCUSSION

The tracing raises a number of important questions,
f none of which can be answered at this time: What is
the cardiac diagnosis? What symptoms and clinical
findings are present? What did previous ECGs show?
What medications is the patient receiving? What are
the values for serum levels of potassium, magnesium,
and of antiarrhythmic drugs?

The basic cardiac rhythm is atrial fibrillation. The
tracing does not display P waves — of either sinus or
ectopic origin — nor atrial flutter waves. Instead, atrial
i activity is represented by the constantly irregular, low-
! amplitude waviness of the isoelectric baseline.

Examination of the tracing for ventricular elec-
trical activity reveals two important findings. First,

I QRS complexes are narrow. This is consistent with
normal intraventricular conduction of atrial fibrilla-
tory impulses that succeed in penetrating the distal
conducting system of the heart. Second, the lengthy
R-R intervals, equivalent to ventricular rates of about
28 to 30 a minute, are a manifestation of significant
AV block. Although QRS complexes, at first glance,
appear to recur regularly, measurement of the R-R
intervals with a set of calipers clearly shows that they
! are not of equal length, but rather vary slightly. This
I finding confirms that the AV block is advanced and
not complete.

Most important, perhaps, are three other ECG
abnormalities: prominent U waves, prolongation of
I the QT interval (0.52 sec), and prolongation of the
QU interval (0.68 sec).

Prominent positive U waves are best seen in pre-
; cordial leads V2 and V4; U waves are inverted in
precordial lead V6. Because the amplitude of the nor-
mal U wave is 5% to 25% of the amplitude of the
preceding T wave, the U wave is termed "prominent"

when it is equal to or taller than the amplitude of the
T wave in the same lead, especially in leads V2 through
V4. The polarity of the normal U wave is usually con-
cordant with the normal T wave. Negative U waves
are nearly always abnormal and their clinical signif-
icance is determined by the clinical situation in which
they are found.

There is no doubt that the QT interval is pro-
longed, but the superimposition of the prominent U
wave in the downstroke of the T wave clearly extends
total repolarization of the ventricles further. QT and
QU intervals prolongation have been correlated with
an increased susceptibility to sudden cardiac death
provoked by malignant ventricular arrhythmias.
Therefore, it is important to identify and correct pos-
sible predisposing and etiologic factors.

When all the ECG findings listed above are taken
into consideration, two major factors are likely re-
sponsible: a combination of multiple electrolyte de-
ficiencies and the concomitant use of antiarrhythmic
drug therapy. The combination of QT and QU pro-
longation with prominent U waves is most often en-
countered when the electrolyte deficiency involves
potassium and magnesium. Intracellular deficiency of
either or both ions may not be accurately reflected in
serum levels until total body stores are markedly re-
duced. Therefore, depletion of both potassium and
magnesium can exist even when serum levels are nor-
mal.

Hypokalemia and hypomagnesemia, alone or in
concert, can exert arrhythmogenic effects on the heart.
These electrolyte abnormalities can also modify the
pharmacologic effects of antiarrhythmic drugs on the
heart. For example, deficiency of either or both elec-
trolytes predisposes to digitalis toxicity by narrowing
the therapeutic range of digitalis; in other words, the
amount of digitalis required to produce toxic effects
is significantly reduced. This is especially true when
these electrolyte deficits are found in patients with
advanced cardiac disease taking digitalis. Other an-
tiarrhythmic drugs that may be partly responsible for
the abnormal findings on the ECG shown here in-
clude the Class I agents: quinidine, procainamide,
and disopyramide.

The "elegant record" has been defined as one

JOURNAL VOL 140 FEBRUARY 13

Specify Adjvinctive

which ''provides a message, both subtle and yet com-
manding." When using an elegant record as a teach-
ing tool, four steps have been suggested: pure de-
scription, statement of the obvious, detection of
unusual or unexpected events, and discussion of "ex-
periments that could be performed to support (or de-
stroy) the explanation offered." In my presentation,
this prescribed approach is used. Unfortunately, the
lack of information makes this tracing elegant, but
incomplete. ■

SELECTED REFERENCES

1. Burch GE, Giles TD: The importance of magnesium deficiency in cardi-
ovascular disease. Am Heart } 1977;94:649-657.

2. Hishida H, Cole JS, Surawicz B: Negative U wave: A highly specific but
poorly understood sign of heart disease. Am / Cardiol 1982;49:2030-2036.

3. Geddes LA: The elegant record. Physiologist 1982;25:448-449.

4. Commerford PJ, Lloyd EA: Arrhythmias in patients with drug toxicity,
electrolyte, and endocrine disturbances. Med Clin North Am 1984;68:1051-
1078.

5. Surawicz B, Knoebel S, Long QT: Good, bad or indifferent. / Am Coll
Cardiol 1984;4:398-413.

6. Stewart DE, Ikram H, Espiner EA, et al: Arrhythmogenic potential of
diuretic-induced hypokalemia in patients with mild hypertension and
ischemic heart disease. Br Heart J 1985;54:290-297.

Dr. Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Department of Medicine at William
Beaumont Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Department of the Army or Department of Defense.

14 JOURNAL VOL 140 FEBRUARY

Each capsule contains 5 mg chlordiazepoxide HCl and 2.5 mg
clidinium bromide

Please consult complete prescribing information, a summary of which
follows:

Indications: Based on a review of this drug by the National Acad-
emy of Sciences— National Research Council and/or other informa-
tion, FDA has classified the indications as follows:

“Possibly” effective: as adjunctive therapy in the treatment of peptic
ulcer and in the treatment of the irritable bowel syndrome (irritaole
colon, spastic colon, mucous colitis) and acute enterocolitis.

Final classification of the less-than-effective indications requires fur-
ther investigation.

Contraindications: Glaucoma; prostatic hypertrophy, benim bladder
neck obstruction; hypersensitivity to chlordiazepoxide HCl and/or
clidinium Br.

Warnings: Caution patients about possible combined effects with alco-
hol and other CNS aepressants, and against hazardous occupations
requiring complete mental alertness {e.g., operating machinery, driving).
Physical and psychological dependence rardy reported on recommended
doses, but use caution in administering Librium® (chlordiazepoxide HCl/
Roche) to known addiction-prone individuals or those who might
increase dosage; withdrawal symptoms (including convulsions) reported
following discontinuation of the drug.

Usage in Pregnancy: Use of minor tranouilizers during first
trimester should ahnost always be avoided because of increased
risk of congeniul malformations as suggested in several studies.
Consider possibility of premancy when instituting therapy.

Advise patients to mscuss therapy if they intend to or do
become pregnant.

As with all anticholinergics, inhibition of lactation may occur.

Adverse Reactions: No side effects or manifestations not seen with
either compound alone reported with Librax. When chlordiazepoxide HCl
is used alone, drowsiness, ataxia, confusion may occur, especially
in elderly and debilitated; avoidable in most cases by proper dosage
adjustment, but also occasionally observed at lower dosage ranges. Syn-
cope reported in a few instances. Also encountered: isolated instances of
skin eruptions, edema, minor menstrual irregularities, nausea and con-
stipation, extrapyramidal symptoms, increased and decreased libido —
all infrequent, generally controlled with dosage reduction; changes in
EEG patterns may appear during and after treatment; blood dyscrasias
(including agranulocytosis), jaundice, hepatic dysfunction reported
occasionally with chlordiazepoxide HCl, making periodic blood counts
and liver function tests advisable during protracted therapy. Adverse
effects reported with Librax typical of anticholinergic agents, i.e., dry-
ness of mouth, blurring of vision, urinary hesitancy, constipation. Con-
stipation has occurred most often when Librax therapy is combined
with other spasmolytics and/or low residue diets.

Roche Products Inc.
Manati, Puerto Rico 00701

P.l 0186

flistiiiie

for the Peacemaker.

In irritable bowel S5mdrome* anxiety can aggravate intestinal symptoms, which may
further intensify anxiety — a distressing cycle of brain/bowel conflict. Librax intervenes with
two well-known compoimds. The Librium® (chlordiazepoxide HCl/Roche) component
safely relieves anxiety. And Quarzan® (chdinium bromide/Roche) provides antisecretory
and antispasmodic action to relieve discomfort associated with intestinal hypermotility.

Dual action — for peace between brain and bowel. Because of possible CNS effects, caution
patients about engaging in activities requiring complete mental alertness. Specify Adjimctive

LIBRi!\X

Each capsule contains 5 mg chlordiazepoxide HCl
and 2.5 mg chdinium bromide

*Librax has been evaluated as possibly effective as adjunctive therapy in the treatment of peptic ulcer and the irritable bowel syndrome.
Copyright ( 1987 by Roche Products Inc. All rights reserved. Please see summary of prescribing information on adjacent page.

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

(

EVALUATION AND MANAGEMENT
OF NASOPHARYNGEAL CARCINOMA

D.L BREEN, MD; PAUL A. BLAIR, MD, FACS

Nasopharyngeal carcinoma is a challenge to the
physician because of its location and capacity for
misdiagnosis. A case report illustrating the ability
of this cancer to mask itself behind neurologic,
otologic, and nasal symptoms is presented.
Evaluation requires a careful head and neck exam,
nasopharyngeal biopsy, and computed tomography
scan. Radiation therapy remains the standard
treatment of these lesions as well as of their neck
metastases. Epstein-Barr virus antibodies can be
sensitive indicators in the diagnosis and
management of nasopharyngeal carcinoma.

N asopharyngeal carcinoma (NPC) is the most
frequently misdiagnosed head and neck malig-
nancy. Although representing less than 2% of head
and neck malignancies, cancers of the nasopharynx j
carry a dismal prognosis. This is related to the pro-
pensity of the tumor to spread into the abundant lym-
phatic drainage of the nasopharynx. Also, the tumor
causes few symptoms when small so, when diag-
nosed, most tumors are already large. ^ ,

The majority of nasopharyngeal cancers are ep- j
idermoid in derivation with lymphomas, adenocar-
cinomas, melanomas, and sarcomas comprising less
than 15%. The three main types of epidermoid car-
cinomas are keratinizing, nonkeratinizing, and un- ]
differentiated. Lymphoepithelioma is a term used to
describe nonkeratinizing and undifferentiated carci-
nomas if abundant lymphocytes are found on histo-
logical sampling. 2 Lymphoepitheliomas are associ-
ated with a better prognosis and higher survival rates. ^

CASE REPORT

A 56-year-old white male came to the Otolaryngology
clinic with complaints of right facial pain, headaches
radiating to base of the head, and nasal obstruction.

16 journal VOL 140 FEBRUARY

Past medical history revealed that the patient had had
pneumatic equalization tubes placed in both ears two
years ago for bilateral serous otitis media and had had
a septoplasty six months ago for nasal obstruction.
No nasopharyngeal biopsy was performed nor was
an unusual nasopharyngeal examination recorded. On
physical examination, the patient had a large mass
obstructing the right choana and a right posterior neck
node measuring 2 cm in diameter. The mass extended
into the nasopharyngeal walls on either side of the
choana but was confined to the nasopharynx. Com-
puted tomography (CT) scan showed no bony in-
volvement or erosion into the base of the skull and
no intracranial extension. Biopsy of the lesion through
the nose confirmed poorly differentiated squamous
cell carcinoma. Epstein-Barr virus (EBV) titer for an-
tibodies to the viral capsid antigen (VCA) was 1:640,
which is seropositive. The patient had a complete
course of radiation for treatment of the primary site
and the extension of the neck. Presently he has no
evidence of disease.

EPIDEMIOLOGY

There are several risk factors related to the develop-
ment of nasopharyngeal carcinoma. The two most
significant epidemiological characteristics of this dis-
ease are race and exposure to the EBV. Southern
Chinese have a risk 118 times average of developing
this cancer whereas for North American-born Chinese
the risk is still seven times average. EBV tests are not
only important diagnostic aids but also are useful in
following the patient for evidence of recurrence.^ EBV
DNA is found in aU three types of NPC.^

Exposure to smoke, chemical fumes, and diet of
salted fish have been linked with NPC. Recently the
role of cigarette smoking as an etiological factor was
found to be consistent with a casual relationship.^

DISCUSSION

The most common presenting symptom is a lump in
the neck; followed by nasal obstruction, epistaxis, and
various otologic complaints (Table 1).^-^ The triad of
hearing loss, maxillary neuralgia, and palatal hemi-
paresis is almost pathognomonic of a nasopharyngeal
neoplasm.

Diagnosis of NPC requires a thorough head and
neck examination, including visual examination of the

TABLE 1

MOST COMMON PRESENTING SYMPTOMS OF
NASOPHARYNGEAL CARCINOMA

Cervical lymph node enlargement

30-70%

Nasal symptoms

epistaxis

obstruction

25%

Otologic symptoms
hearing loss
infection
earache
tinnitus
dizziness

20-40%

Cranial Nerve Dysfunction

8-25%

nasopharynx by mirror or endoscope, and an evalu-
ation of cranial nerve function. Nasopharyngeal bi-
opsy can usually be done transnasally in the office or
clinic with use of topical anesthesia. CT scan of the
complete extent of the lesion is important to deter-
mine bony or intracranial extension. Lymphatic drain-
age from the nasopharynx is directly into lateral re-
tropharyngeal nodes with connection to nodes around
the jugular foramen and to cranial nerves IX through
XII. Neck drainage commonly leads to enlargement
of the jugulodigastric and posterior cervical nodes in
the spinal accessory chain. An enlarged posterior neck
node should alert the physician to perform a thorough
search of the nasopharynx, the most common site of
origin of the primary leading to posterior triangle node
involvement.

Distant metastasis is most frequently to bone,
then to lung, liver, and distant lymph nodes. Al-
though chest roentgenograms and liver profile are
routinely obtained, bone scans are reserved for those
patients presenting with bone symptoms or elevated
serum calcium levels.

Treatment of NPC consists of from 5000 to 7500
rads to the primary and the neck as weU as intracav-
itary boosts with radium seed implants.^ Referral for
radiation therapy should be preceded by a careful
dental evaluation and treatment as needed. Surgery
is not recommended due to the location of the tumor
at the base of the skull in the nasopharynx — a major
obstacle to resection.

Staging has been shown to be a major indicator
in prognosis, with extension beyond the nasopharynx

JOURNAL VOL 140 FEBRUARY 17

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VALIUM

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REMEMBER TO WRITE “DO NOT SUBSTITUTE. ”
IT PROTECTS YOUR DECISION.

The cut out "V" design is a registered trademark of Roche Products Inc.

TABLE 2

STAGING OF NASOPHARYNGEAL CARCINOMA
ACCORDING TO TNM SYSTEM

T, one site in nasopharynx involved

Tz two sites in nasopharynx involved (generally the posterior-
superior or lateral walls)

T 3 extension into the nasal cavity or outside the nasopharynx

T 4 invasion of bone and/or cranial nerve involvement

No no palpable node

Ni single lymph node less than 3 cm

Na a) single node 3-6 cm

b) multiple homolateral nodes, each less than or equal to 6
cm

N 3 a) homolateral node greater than 6 cm

b) bilateral nodes

c) contralateral nodes

and involvement of neck nodes highly negative prog-
nosticators. The primary tumor/regional nodes/dis-
tant metastasis classification is presented in Table 2.
Five-year survival rates range from 80% to 90% for
Stage I, 60% to 70% for Stage 11, 40% to 50% for Stage
III, and 10% to 40% for Stage IV. ^ Recent studies with
adjuvant chemotherapy show promising responses in
Stage III and IV disease.®

Recurrences in the nasopharynx are treated with
either surgery or radiation boost, whereas neck re-
currences are best treated with radical neck dissec-
tion.

EPSTEIN-BARR VIRUS TITERS

The seropositive rates in NPC patients for EBV as-
sociated antibodies — early antigen (EA) and VGA —
range from 42% to 100%.^ Of this group, anti-VGA
IgA and anti-EA IgG are the most sensitive indicators
in the diagnosis and management of patients with
NPG.i"

A total of 85% of patients with nonkeratinizing
and undifferentiated carcinoma types have antibody
responses versus a 16% response in controls.^ In con-
trast, only 35% of keratinizing squamous cell patients
had positive responses. This makes anti-VGA IgA and
anti-EA IgG important diagnostic tools for following
NPG patients with the two most serious types of na-
sophryngeal carcinoma. As the patient enters remis-
sion, response rates fall to 18%, while response rates
with recurrence or distant metastases, increase to 85%
to 100%.

Serial anti- VGA and anti-EA titers after radiation
therapy can alert the physician to occult recurrence
or metastases. Gontinued high viral titers after radio-
therapy can be interpreted as indicating the presence
of residual disease.

SUMMARY

NPG is a formidable opponent to the head and neck
cancer surgeon mainly because of its late presentation
and propensity for misdiagnosis. A good head and
neck exam, nasopharyngeal biopsy, and GT scan of
the nasopharynx complete the diagnostic work-up.
The mainstay of treatment is radiation therapy with
excellent cure rates if started early. The use of EBV
antibody titers is a sensitive method for detecting oc-
cult disease. ■

REFERENCES

1 . Neel HB III: A Prospective Evaluation of Patients With Nasopharyngeal
Carcinoma: An Overview. / Otolaryngol 1986;15:137-144.

2. Fox R and Graham WP. Carcinoma of the Nasopharynx and Posterior
Pharyngeal Wall. Surg Clin North Am 1986;66:97-108.

3. Rahima M et al. Carcinoma of the Nasopharynx: An Analysis of 91 Cases
and a Comparison of Differing Treatment Approaches. Cancer 1986;58:843-
849.

4. Neel HB et al. Application of Epstein-Barr Virus Serology to the Diag-
nosis and Staging of North American Nasopharyngeal Carcinoma. Oto-
laryngol Head Neck Surg 1983;91:255-262.

5. Raab-Traub N et al. The Differentiated Form of Nasopharyngeal Carci-
noma Contains Epstein-Barr Virus. DNA. Int J Cancer 1987;39:25-29.

6. Mabuchi K, Bross DS and Kessler II. Cigarette Smoking and Nasopha-
ryngeal Carcinoma. Cancer 1985;55:2874-2876.

7. Schabinger P et al. Carcinoma of the Nasopharynx: Survival and Patterns
of Recurrence. Int J Radiat Oncol Biol Phys 1985;11:2081-2084.

8. Chatani M et al. Radiation Therapy for Nasopharyngeal Carcinoma.
Retrospective Review of 105 Patients Based on a Survey of Kansai Cancer
Therapist Group. Cancer 1986;57:2267-2271.

9. Lynn T-C et al. Epstein-Barr Virus — Associated Antibodies and Serum
Biochemistry in Nasopharyngeal Carcinoma. Laryngoscope 1984;94:1485-
1488.

10. Neel HB III, Pearson GR, and Taylor WF. Antibodies to Epstein-Barr
Virus in Patients With Nasopharyngeal Carcinoma and in Comparison
Groups. Ann Otol Rhinol Laryngol 1984;93:477-481.

Drs. Breen and Blair are from the Dept of Otolaryngology-Head and
Neck Surgery at Tulane University School of Medicine in New Orleans.

Reprint requests should be sent to Paul A. Blair, MD, Department of
Otolaryngology-Head and Neck Surgery, 1430 Tulane Ave,

New Orleans, LA 70112.

JOURNAL VOL 140 FEBRUARY 21

CAT FMDAR

March

March 6-11

9th Annual Mammoth Mountain Emergency Medicine,

Mammoth Lakes, California. Contact: Medical Conferences, Inc,
CME Travel Service, 1615 S Mission Road, Suite 3, Fallbrook, CA
92028; (714)650-4156.

March 7-9

World Congress III on Cancers of the Skin, The Lincoln
Hotel Post Oak, Houston. Contact: University of Texas M.D.
Anderson Hospital and Tumor Institute, Office of Conference Ser-
vices HMB 131, 1515 Holcombe Blvd, Houston, TX 77030;
(713)792-2222.

1988 Annual Meeting
Louisiana State Medical Society
March 10-13, Lake Charles

March 12-27

Australia/New Zealand - Diagnostic Imaging Down Under,

Australia and New Zealand. Contact: Medical Seminars Inter-
national, 21915 Roscoe Blvd, Suite 222, Canoga Park, CA 91304;
(818)719-7380.

March 14-18

March 16-19

Highlights in Women's Health Care, Orlando, Florida. Con-
tact: Susan Larson, Director, Scott and White Office of Continu-
ing Medical Education, 2401 South 31st St, Temple, TX 76508;
(817)774-4083.

March 17-18

Assessment of Clinical Competence in Specialty Medicine,

Toronto Hilton Harbour Castle Hotel, Toronto. Contact:
American Board of Medical Specialties, One Rotary Center #805,
Evanston, IL 60201.

March 17-19

Advanced Concepts in Rigid Skeletal Fixation, Delta Moun-

tain Inn, Whistler, British Columbia. Dr. M. Kaburda, Suite
208, 600 Royal Ave, New Westminster, BC; (604)524-1301.

March 17-20

Hair Replacement Surgery, Los Angeles. (Zontact: American
Academy of Facial Plastic and Reconstructive Surgery, 1101 Ver-
mont Ave NW, Suite 404, Washington, DC 20005.

March 19-27

A Study Tour in England on Public and Private Care In-
novations for the Aged, London, Oxford, and Canterbury.
Contact: Pat Ashton, Holbrook Travel, 3540 NW 13th Street,
Gainesville, FL 32609; (800)451-7111.

March 25-26

Advances in Emergency Medicine: Toxicology and Infec-
tious Disease, Mission Bay, California. Contact: Continuing
Education in Health Sciences, UCLA Extension, PO Box 24901,
Los Angeles, CA 90024; (213)825-7257.

March 25-27

Rigid Fixation of the Facial Skeleton, Walt Disney World
Village, Lake Buena Vista, Florida. Contact: Mary Appleton,
Dept of Oral and Maxillofacial Surgery, Northwestern University
Dental School, (312)908-5243.

March 26 - April 12

Orthopedic Emergencies, Waiohai & Poipu Beach Hotels,
Kauai, Hawaii. Contact: Edith S. Bookstein, Conference Manage-
ment Associates, PO Box 2586, La Jolla, CA 92038; (619)454-3212.

March 28-30

NIH Consensus Development Conference/Kidney Stones:
Prevention and Treatment, Bethesda, Maryland. Contact:
Conference Registrar, Prospect Associates, Suite 500, 1801 Rockville
Pike, Rockville, MD 20852; (301)468-MEET.

April

April 8-10

Louisiana Psychiatric Association/Mississippi Psychiatric
Association Joint Meeting, Natchez, Mississippi. Charlene
Smith, Louisiana Psyciatric Association, PO Box 15765, New
Orleans, LA 70175; (504)891-1030.

April 13-17

4th Annual Family Medicine Review, Austin, Texas, Dept
of Continuing Medical Education, Scott & White, 2401 South 31st
St, Temple, TX 76508; (817)774-2350.

22 JOURNAL VOL 140 FEBRUARY

April 20-24

2nd Annual Review Course in Critical Care Medicine,

Washington, DC. Contact: Svetlana Lisanti, Program Coor-
dinator, Center for Bio-Medical Corhmunication, (201)385-1808.

April 22-24

3rd International Interdisciplinary Conference on Hyperten-
sion in Blacks, Baltimore. Contact: Cecile Cate, Conference Coor-
dinator, International Society on Hypertension in Blacks, 69 Butler
St SE, Atlanta, GA 30303; (404)589-3810.

April 23-24

The Cutting Edge 1988/Innovations in Psychotherapy: Help-
ing Individuals and Couples to Change, Hotel Del Cor-
onado, Sna Diego. Contact: Office of Continuing Medical Educa-
tion, UC San Diego School of Medicine, La Jolla, CA 92093;
(619)534-3940.

May

May 2-4

NIH Consensus Development Conference: Cochlear Im-
plants, Bethesda, Maryland. Contact: Conference Registrar, Pro-
spect Associates, Suite 500, 1801 Rockville Pike, Rockville, MD
20852; (30D468-MEET.

May 4-6

6th Regions II & III High Blood Pressure Conference/New
Challenges — Creative Solutions, Richmond, Virginia. Paula
A. Ciaverella or Joann T. Richardson, Virginia Dept of Health,
Division of Chronic Disease Control, 109 Governor St, Madison
Bldg, Richmond, VA 23219; (804)786-4065.

May 5-7

The National Conference on Health Care Leadership and
Management, Sheraton Harbor Island, San Diego. Contact:
Sherry Mason, American Academy of Medical Directors, 4830 W
Kennedy Blvd, Suite 648, Tampa, EL 33609-2517; (813)287-2000.

May 13 - June 3

Cruise/ Seminar on Risk Management and Comparative
Medicolegal Issues, Hong Kong, China, and Japan. Inter-
national Conferences, Suite C, 189 Lodge Ave, Huntington Sta-
tion, NY 11746; (800)521-0076, (516)549-0869.

June

June 1-4

9th Conference on Computer Applications in Radiology,

HUton Head Island, South Carolina. Contact: Ms. Janice Ford,
Continuing Education Coordinator, Dept of Radiology Hospital of
the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA
19104; (215)662-6904, (215)662-6982.

June 16-18

33rd Annual Great Smokey Mountain Pediatric Seminar,

Park Vista Hotel, Gatlinburg, Tennessee. Contact: Dr. San-
dra Loucks, University of Tennessee Medical Center, Dept of
Pediatrics, 1924 Alcoa Hwy, Knoxville, TX 37920; (615)544-9331.

JOURNAL VOL 140 FEBRUARY 23

MICROSURGERY 1987:

THE LSU EXPERIENCE

JAMES W. WADE, MD; ROY F. BRABHAM, MD;
L. FRANKLYN ELLIOTT, MD

24 JOURNAL VOL 140 FEBRUARY

Microsurgery was introduced into the Louisiana
State Lfniversity program of Plastic and
Reconstructive Surgery in 1978. Since 1983, 78 free
tissue transfers have been performed in 75 patients
at LSU-associated teaching hospitals with a success
rate of 92% . Much has been accomplished in the
realm of refinement of microsurgical techniques
such that morbidity of both donor site and
recipient site is minimized. This paper attempts to
outline indications for and selection of free tissue

transfer.

W ITH AN EVER-INCREASING demand for safe and
effective means of providing coverage to trau-
matic and surgical defects, free tissue transfer has
become a viable approach toward management of such
problems.^ Since the introduction of microsurgery into
the LSU program of Plastic and Reconstructive Sur-
gery in the late 70s, considerable success has been
achieved in terms of both immediate and late recon-
struction of difficult wounds and anatomic defects by
utilizing free tissue transfer. Over the past four years,
we have specifically addressed our efforts and atten-
tions toward refinement of standard microsurgical
techniques to provide not only effective bony/soft tis-
sue reconstruction but also optimal functional and
cosmetic results.

Our microsurgical experience as a whole has dealt
largely with two parameters, namely free tissue trans-
fer and replantation. The objective of this paper, how-
ever, is to outline the indications and selection of
specific flaps available for free tissue transfer. This
entity itself offers significant versatility in selection of
the transferred tissue to accommodate a specific de-
fect with optimal results in terms of both function and
cosmetic appearance of donor and recipient sites (Ta-
ble 1). Since July 1983, we have performed 78 free
tissue transfers at the LSU-associated teaching hos-
pitals. We have had six failures for a success rate of
[ 92%, exceeding the internationally accepted 85% to

I 90% successful transfer figures.^ Three of the failed
transfers were in host-compromised patients and may
possibly represent errors in patient selection. Post-
I operative complications, aside from flap failure, have
required re-operation in eight instances in the im-
mediate post-operative period. Other complications

TABLE 1

FREE TISSUE TRANSFER —

AVAILABLE TISSUES |

Skin

Muscle-skin

Fascia

Bone

Skin-fascia

Omentum

Muscle

Jejunum

TABLE 2

FREE TISSUE TRANSFER -

- 78 FLAPS

No.

Failed

Success
Rate (%)

Latissimus Dorsi

Forearm Fasciocutaneous

100

Scapular Fasciocutaneous

100

Gracilis

100

Jejunum

87.5

Omentum

100

Rectus Abdominis

Tensor Fascia Lata

100

Fibula

100

Iliac Crest

Temporalis Fascia

100

Toe to Hand

100

Thoracic Fascia

100

92%

have been limited to seroma formation at donor sites
and superficial infections.

There is a vast array of flaps available for free
tissue transfer and the variety of flaps utilized in this
series demonstrates the versatility and refinements of
the science of free tissue transfer over the last few
years (Table 2). Objectives of transfer are first to pro-
vide coverage of a specific defect followed by resto-
ration of function and cosmetic appearance. Desired
thickness, presence or absence of skin and/or bone,
size of defect, anatomic location of recipient site, and
future requirements (eg, weight-bearing, sensibility,
delayed bone grafts) are all taken into account in se-
lecting an appropriate donor tissue for free transfer.
Additional considerations, by no means of little im-
portance, are donor site morbidity and cosmetic ap-
pearance. In the early days of free tissue transfer these
latter considerations were of less significance than
they are today.

JOURNAL VOL 140 FEBRUARY 25

Fig 1. Open tibia fracture with exposed bone, ten-
don, vessels and deficient soft tissue cov-
erage.

Recipient sites for transfer have been primarily
in the lower extremity where defects in the distal third
of the leg have in the past been relegated to ampu-
tation in many instances (Table 3, Figs 1, 2). Especially
amenable to free tissue transfer is exposed bone with
chronic osteomyelitis, a condition for which both clin-
ical and laboratory evidence exists validating trans-
ferred revascularized muscle (coupled with adequate
debridement) provides for expeditious and effective
healing (Figs 3, 4),^' ^ In the absence of infected tissues,
an appropriate alternative to free muscle transfer is
revascularized fascia or fasciocutaneous flaps which
provide a durable yet thin cover to soft tissue defects.
Transfers to the lower extremity have included those

26 JOURNAL VOL 140 FEBRUARY

Fig 2. Follow-up of rectus abdominis free flap with
skin graft after 14 months.

to weight-bearing areas of the foot and these have
withstood the daily trauma of ambulation. Some can
be innervated at the time of transfer to allow for return
of protective and tactile sensibility.

We have not, however, limited our experience to
the lower extremity and we have utilized free tissue
transfer for defects to the upper extremity as well as
the head and neck. These areas are often found to be

TABLES

FREE TISSUE TRANSFER —

RECIPIENT SITES

Number

Head & Neck

Upper Extremity

Lower Extremity

Fig 3. Chronic osteomyelitis following open tibia
fracture.

Fig 4. Follow-up of latissimus dorsi free flap with
skin graft after six months.

in need of reconstruction in response to both trau-
matic and surgical defects. One area of particular im-
portance is the cervical esophagus where ablative sur-
gery has previously resulted in a considerable
functional and cosmetic defect requiring cervical
esophagostomy and gastrostomy for feeding and se-

Fig 5. Pre-operative barium esophagogram dem-
onstrating subtotal cervical esophageal oc-
clusion secondary to recurrent laryngeal
carcinoma.

cretion management — results adversely affecting
quality of life in these unfortunate patients. With
transfer of a segment of jejunum to restore continuity
to the alimentary canal, patients are able to eat and
handle their own secretions without difficulty, and
thereby an improvement in the quality of life is
achieved (Figs 5-7).^' ^ Cutaneous defects of the face
and hand require thin, pliable tissues with an ac-
ceptable cosmetic appearance. Free transfers common
to these areas are usually derived from the skin/fascia
of the forearm or the fascia alone from either the arm,
back, or temple coupled with a skin graft.

Operative procedures of this magnitude are not
without complication, but fortunately most can be
effectively managed without loss of the transferred
tissue or an increase in hospital stay. With added
experience, operative time averages four and one-half
hours. The patient is maintained in an intensive care
setting 48 to 72 hours post-operatively and the ex-
pected date of discharge is 12 to 14 days following
free tissue transfer. We feel that this relatively short
post-reconstruction hospital stay significantly de-
creases the overall cost of hospitalization in patients
with difficult reconstructive problems.

SUMMARY

It is our feeling that microsurgery in the realm of free ►
JOURNAL VOL 140 FEBRUARY 27

Fig 6. Segment of jejunum as free transfer in place
in neck foliowing surgicai resection of re-
current carcinoma (tracheostome is at bot-
tom).

Fig 7. One month post-operative follow-up esoph-
agogram demonstrating patency and mu-
cosai folds of jejunum in neck.

28 JOURNAL VOL 140 FEBRUARY

tissue transfer has much to offer to the surgical com-
munity and is relevant to all specialties within it. With
greater experience and attention to detail, refinements
have been and will continue to be made in efforts to
provide optimal patient care and management. ■

REFERENCES

1. Daniel RK, Taylor GI: Distant transfer of an island flap by microvascular
anastomoses. Plast Reconstr Surg 1973;52:111-117.

2. Shaw WW: Microvascular free flaps: The first decade. Clin Plast Surg
1983;10:3-20.

3. Mathes SJ, Alpert BS, Chang N: Use of the muscle flap in chronic osteo-
myelitis: Experimental and clinical correlation. Plast Reconstr Surg
1982;69:815-828.

4. Ger R: Muscle transposition for the treatment and prevention of chronic
post-traumatic osteomyelitis of the tibia. / Bone Joint Surg 1977;59A:784-
791.

5. Jurkiewicz MJ: Vascularized intestinal graft for reconstruction of the cer-
vical esophagus and pharynx. Plast Reconstr Surg 1965;36:509-517.

6. McConnel MS, Hester JR, Nahai F, et al: Free jujenal grafts for recon-
struction of pharynx and cervical esophagus. Arch Otolaryngol Head Neck
Surg 1981;107:476-481.

Dr. Wade received his medical degree from LSU School of Medicine in
New Orleans in 1978 and completed a general surgery residency at the
Medical College of Georgia and plastic surgery training at LSU. He is
currently a plastic and reconstructive surgeon in private practice in
Baton Rouge and holds a clinical appointment within the Dept of
Surgery, Division of Plastic Surgery at LSU Medical Center. He is also
affiliated with Our Lady of the Lake Regional Medical Center in

Baton Rouge.

Dr. Brabham is a graduate of the LSU School of Medicine in Shreveport
and completed general surgery and plastic surgery training at the
University of Wisconsin. He is presently in private practice
in Baton Rouge and is affiliated with Our Lady of the
Lxike Regional Medical Center.

Dr. Elliott completed his medical education at Vanderbilt and his
general surgery residency with Tulane. He followed with plastic surgery
training at Emory University and held a clinical appointment with the
LSUMC Department of Plastic Surgery. He has recently moved to
Atlanta where he is in private practice.

Reprints will not be available.

Medicolegal Hotline

legal advice at no charge

A free service from the LSMS
which will confidentially answer
your questions about:

• PPOs and HMOs

• Malpractice

• Release of patient records

and information

• Informal consent

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• Receipt of subpoena

• Reporting child abuse

FOR PHYSICIANS ONLY
Please limit calls to medicolegal issues. Routine
legal matters should be referred to your attorney.

Adams & Reese, Attorneys at Law

Edward J. Rice or Robert J. Conrad, Jr.

(504) 581 -3234

JOURNAL VOL 140 FEBRUARY 29

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Eighteen physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
November, 1 987. This award is presented by the American Medical Association to physicians who have voluntarily
completed 1 50 hours of continuing medical education during a consecutive three-year time period. Of these 1 50
hours, at least 60 must be in AMA/PRA Category 1 . These eighteen individuals and the cities in which they reside
are presented below.

Alexandria

John Allen Baldridge, MD*

Keith Alan Holmes, MD*

Baton Rouge

Chester C. Coles, Jr., MD
Ngo Khai, MD
Gilbert B. Meyers, MD
Reza Sheybani, MD*

Buras

Philippe Logaglio, MD*

Covington

William James Mitchell, MD

Kenner

Michael John Jennings, MD

Metairie

Leon Lapleau Mclntire, MD*

New Iberia

Edward W. Dauterive, MD

New Orleans

Kenneth Allen Bell, MD
Robert Charles Fortenberry, MD
John A. Kalmar, MD
Larry Edward Millikan, MD
Ernest O. Svenson, MD

Shreveport

David Thomas Henry, MD
Jack Selwyn Resneck, MD

* These individuals are members of the Louisiana State Medical Society

30 JOURNAL VOL 140 FEBRUARY

SONOGRAPHIC EVALUATION OF
ACUTE BACTERIAL MENINGITIS

KRISHNA GRAVOIS, MD

A cute bacterial meningitis may result in compli-
cations despite appropriate treatment. Cribside,
portable, real-time ultrasound can be easily per-
formed without transporting a sick infant who may
be on a mechanical ventilator and other life support-
ing devices. The examination is safe and low-
cost as compared to computed tomography (CT),
and requires no sedation. Intracranial changes can be
easily and repeatedly demonstrated. Sonographic
findings vary from normal (Figs 1, 2) to evidence of
echogenic sulci, ventriculomegaly, extra-axial fluid
collection (EAF),^'^ diffuse or localized intense paren-
chymal echos, ventriculitis,^' ^ gyral infarction,^ and
brain abscess.^' ^

MATERIALS AND METHODS

Between 1984 and 1987, approximately 60 proven cases
of acute bacterial meningitis were treated at our hos-
pital. Complicated cases were evaluated mostly by
cranial CT, but recently we have been using portable
real-time ultrasound (7.5 MHz transducer) and ob-
taining sagittal and coronal scans at cribside without
the need to transport to a sick baby.

CASE REPORT

An infant of 38 weeks gestation, weighing 7 lbs 4 oz
was born without complication. During that stay, the
baby had several spells of apnea for which cranial
ultrasound yielded results normal for a neonate (Figs
1, 2). The baby was discharged on the seventh day
in good condition.

Approximately two months after discharge, the
baby was readmitted for upper respiratory infection,
vomiting, diarrhea, and dehydration. Symptomatic
treatment was initiated, but on the next day the baby
developed a stiff neck and constant crying. Blood cul-
ture grew Hemophilus influenzae type b. Spinal punc-
ture was performed with cerebrospinal fluid findings
of a RBC count of 500/ (jlL, a WBC count of 575/ |xL with
83% neutrophils and 17% lymphocytes, a glucose level
of 1 mg/dL, and a protein level of >380 mg/dL. Gram
stain showed many bacteria.

Besides the bacterial meningitis due to septi-
cemia, the baby developed acute renal failure, acute
respiratory failure, and pericarditis. Chest x-ray dem-
onstrated cardiomegaly. An echocardiogram revealed ►

JOURNAL VOL 140 FEBRUARY 31

ACKNOWLEDGMENTS

My thanks to Martha Morgan for technical assistance,
Vickie Mayham for manuscript preparation, and Erin
Patrick for photography.

REFERENCES

1. Han BK, Babcock D, McAdams L, et al: Bacterial meningitis in infants:
Sonographic findings. Radiology 1985;154(3):645-650.

2. Rosenberg HK, Levine RS, Stoltz K, et al: Bacterial meningitis in infants:
Sonographic features. AJNR 1983;4(3):822-825.

3. Reeder JD, Sanders RC: Ventriculitis in the neonate: Recognition by son-
ography. AJNR 1983;4(1):37-41.

4. Hill A, Shakelford GD, Volpe JJ, et al: Ventriculitis with neonatal bacterial
meningitis: Identification by real time ultrasound. / Pediatr 1981;99(1):133-
136.

5. Babcock DS, Han BK: Sonographic recognition of gyral infarction in men-
ingitis. AJR 1985; 144(April): 833-836.

6. Fisher RM, Lipinski JK: Ultrasonograph assessment of infectious men-
ingitis. Clin Radiol 1984;35:267-273.

Dr. Gravois is a radiologist affiliated with Earl K. Long Memorial
Hospital in Baton Rouge. She is also an instructor in radiology at
LSU School of Medicine in New Orleans.

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Contact: Current Concept Seminars

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(305) 966-1009

ON CALL

physician phone directory

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( 504 ) 561-1033

( 800 ) 462-9508

LSMS Office of Governmental Affairs

( 504 ) 383-8500

( 800 ) 624-1247

LSMS Medicolegal Hotline

( 504 ) 581-3234

American Medical Association

( 312 ) 645-5000

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( 504 ) 831-3756

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( 800 ) 423-4992

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Provider Inquiry Center

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34 JOURNAL VOL 140 FEBRUARY

GOLD-INDUCED PNEUMONITIS

BRUCE A. BAETHGE, MD; ROBERT E. WOLF, MD, PhD

Gold-induced pneumonitis is an uncommon
complication of chrysotherapy in rheumatoid
arthritis (RA). Since RA patients may suffer from a
variety of pulmonary problems, prompt diagnosis
is essential for proper management. A report of a
patient with gold-induced pneumonitis is
presented and discussed.

P ULMONARY COMPLICATIONS are common in rheu-
matoid arthritis (RA). Pleuritis, pulmonary nod-
ules, interstitial fibrosis, and vasculitis are recognized
features of the disease.^ Patients with RA also develop
frequent pulmonary infections and complications of
drug therapy.^ When RA patients present with pul-
monary disease, it becomes a challenging problem for
the clinician to establish the correct diagnosis and
institute proper therapy.

Gold-induced pneumonitis was first reported in
1948^ but did not become generally recognized until
Winterbauer, et al described two cases with lung biop-
sies in 1976.^ More than 60 cases have subsequently
been reported estabhshing the characteristic clinical
and pathological features of the syndrome.^ Since pul-
monary toxicity from gold therapy is uncommon, it

may not be considered or recognized when rheu-
matoid patients initially develop respiratory symp-
toms. We present a case which demonstrates the char-
acteristic clinical features of the syndrome and discuss
the etiology, diagnosis, and management.

CASE REPORT

A 73-year-old white woman was admitted to the Uni-
versity Hospital at LSU Medical Center in Shreveport
on Aug 1, 1985 for evaluation of progressive respi-
ratory distress and nonproductive cough. One year
prior to admission, she had developed symmetrical
polyarthritis and the diagnosis of RA was established.
When symptoms did not respond to non-steroidal
anti-inflammatory drugs, intramuscular chrysother-
apy was begun on March 20, 1985. After weekly test
doses of 10 mg and 25 mg, she received 50 mg of
aurothioglucose weekly until the date of admission
(total dose 835 mg). In early July, she began to ex-
perience wheezing with nonproductive cough and was
given the diagnosis of bronchitis. Oral ampidllin was
then given for 10 days without improvement.

Her past medical history was remarkable for mild
chronic obstructive pulmonary disease. She denied
fever, chills, night sweats, or pleuritic pain. The only ►

JOURNAL VOL 140 FEBRUARY 35

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medication she had routinely received before admis-
sion besides gold was ibuprofen 600 mg three times
each day. She had a history of cigarette smoking of
a pack a day for 44 years but had stopped 15 years
ago. A chest roentgenogram taken in March 1985 was
read as "normal for age."

Admission physical examination revealed a thin
elderly woman using accessory muscles with breath-
ing. Her blood pressure was 128/70 mm Hg, pulse 80
beats/min, respiration 34/min; she was afebrile. Lung
examination revealed diffuse bilateral wheezes. Rales
were present at the bases with dullness to percussion
on the right side. Cardiac examination was normal
with the absence of any murmur, gallop, or rub. The
rest of the physical examination was essentially nor-
mal except for the joint findings of rheumatoid ar-
thritis.

Admission laboratory studies were normal except
for the arterial blood gases. There was marked hy-
poxia on room air with pH 7.41 PO 2 40 mm Hg, PCO 2
49 mm Hg, and O 2 saturation of only 74%. The ad-
mission chest roentgenogram revealed bilateral patchy
infiltrates and pleural effusions (Fig 1). Fluid obtained
by thoracentesis was an inflammatory exudate with
a WBC count of 3,500 with 35% polymorphonuclear
leukocytes and 65% lymphocytes. Smears for bacteria,
mycobacteria, and fungi were negative as were all
cultures and serologic tests for infection. An inter-
mediate skin test for tuberculosis was negative with
a positive mumps control.

On Aug 5, 1987, a closed needle pleural biopsy
was performed on the right side which revealed only
chronic, non-specific inflammation. The patient's
symptoms persisted despite treatment with bron-
chodilators and supplemental oxygen. On Aug 15,
1987, she underwent an open biopsy of the right lung.
The histopathology revealed numerous giant cells,
foamy histiocytes, and interstitial fibrosis with some
lipid deposits in the interstitial spaces. The biopsy was
interpreted as representing an organizing pneumo-
nitis. All stains for bacteria, mycobacteria, and fungi
were negative. Based on the clinical history and path-
ologic findings, a diagnosis of gold pneumonitis was
made. Chrysotherapy was discontinued. The patient
was started on prednisone 40 mg/day and experi-
enced dramatic improvement in symptoms. Spi-
rometry obtained Aug 22, 1987 revealed severe re-
strictive disease with a forced expiratory volume at
one second of 0.59 L (34% of predicted) and with a

Fig 1. Chest roentgenogram revealing bilateral
patchy infiltrates and pleural effusions.

forced vital capacity of 0.9 L (36% of predicted); with
the reduced flow rate compatible with mild obstruc-
tive ventilating impairment. By Aug 23, 1987, the pa-
tient was improved enough for discharge.

Frequent outpatient examinations documented
improvement of respiratory symptoms and arterial
blood gas determinations. The prednisone was grad-
ually tapered over the next four months. A repeat
chest roentgenogram on Nov 20, 1986 (Fig 2) revealed
only residual interstitial changes. All pulmonary
symptoms had resolved.

DISCUSSION

Gold-induced pneumonitis is an uncommon disorder
with an incompletely understood pathogenesis. A re-
cent article reviewing a 47-year experience with gold
therapy in 1,019 rheumatoid patients did not describe
a single case.^ A multicenter study from Finland iden-
tified 16 cases of gold-induced pneumonitis over a 10-

JOURNAL VOL 140 FEBRUARY 37

Fig 2. Repeat chest roentgenogram revealing re-
siduai interstitiai changes.

year period.^ The syndrome usually occurs with the
injectable gold salts, gold sodium thiomalate or au-
rothioglucose; however, there is one report of a case
with the oral preparation auranofin/ While there is
no way to predict which patients are at risk, there is
evidence that genetic factors may contribute to the
development of gold pneumonitis. Partanen, et al have
found that patients with RA and gold pneumonitis
express two extended human lymphocyte antigen
haplotypes in higher frequencies than controls.® The
clinical manifestations and pathological findings of
the syndrome strongly suggest that it is a hypersen-
sitivity reaction to gold and not a feature of rheu-
matoid disease. This concept is supported by reports
of cases of gold pneumonitis occurring in patients
with osteoarthritis erroneously treated with gold.^ The
syndrome also has recurred when patients were re-
challenged with gold.® Although pathogenesis of the

lung injury has not been studied extensively, gold-
stimulated peripheral blood lymphocytes from pa-
tients with gold pneumonitis elaborate lymphokines
and chemotactic factors,^ suggesting that cell- mediated
immunity may play a role.

The characteristics of patients with gold-induced
pneumonitis have been described in a recent review.
The individuals are usually women with the mean
age of 53, who had received an average of 582 mg of
gold (range 120 mg to 1660 mg) before symptoms
appeared. Dyspnea on exertion has been the pre-
senting complaint in 95% of patients, while less than
half of the patients will present with cough or fever.
Other complications of gold therapy are usually ab-
sent although gold dermatitis has appeared with pul-
monary symptoms in some patients.^® Physical ex-
amination usually reveals only tachypnea and crepitant
basilar rales. The chest roentgenographic findings are
non-specific with diffuse, usually bilateral, interstitial
and/or alveolar infiltrates present together with patchy
consolidations.

There are no characteristic laboratory findings.
Peripheral blood leukocytosis and eosinophilia are
found in only about half of the patients. Serologic
studies are not helpful. The erythrocyte sedimenta-
tion rate is usually elevated, and 59% of the patients
have been positive for rheumatoid factor. There is one
report of hypogammaglobulinemia occurring with gold
pneumonitis.^^ The majority of patients have arterial
blood gas abnormalities with hypoxia and hypocarbia
being common. There is a report of ventilatory failure
with hypercarbia.^° Pulmonary function testing has
consistently demonstrated a restrictive ventilatory
pattern with reduced single breath carbon monoxide
diffusion capacity. Serial pulmonary function testing
has shown improvement in the restrictive defect after
withdrawal of gold and initiation of glucocorticoid
therapy.

The most common pathologic finding in the lung
can be described as fibrosing alveolitis. Differing pat-
terns of alveolar inflammation with infiltration of lym-
phocytes, plasma cells, and histiocytes and interstitial
fibrositis have been reported.^® Reactive type II alveo-
lar cell hyperplasia occurs and can be prominent
enough to initially suggest the diagnosis of malig-
nancy.^® In one patient, indirect immunofluorescence
has demonstrated subepithelial deposits of IgG, and
scanning electon microscopy has demonstrated gold

38 JOURNAL VOL 140 FEBRUARY

deposits. Unfortunately the histologic findings are
not diagnostic for gold pneumonitis since all of the
changes described can be found with primary rheu-
matoid lung disease.

The differential diagnosis of gold pneumonitis
includes primary rheumatoid lung disease, chronic
pulmonary infection, and malignancy. The latter two
diagnoses can usually be excluded by negative stains
and cultures for pathogens and by tissue histopath-
ology. Since the pathologic appearance of gold-
induced pneumonitis can be similar to rheumatoid
interstitial lung disease, the clinician must rely on
clinical features and suspicion to make the diagnosis.

Recently, the use of bronchoalveolar lavage (BAL)
has been advocated for diagnosis. Evaluation of the
lavage fluid from gold pneumonitis patients reveals
an increased number of lymphocytes compared to
normal controls while increased numbers of poly-
morphonuclear leukocytes are usually found in pri-
mary rheumatoid interstitial lung disease.^ Although
this technique appears promising, the clinical use-
fulness of BAL in gold-induced pneumonitis remains
to be established.

The most useful diagnostic and therapeutic ma-
neuver is observation of the patient after stopping
gold. The diagnosis can usually be made when the
following criteria are found: acute to subacute onset
of symptoms during early stages of gold therapy; dif-
fuse usually bilateral pulmonary infiltrates; improve-
ment after discontinuation of gold, treatment with
steroids or both; and no recurrence of the disease in
follow-up. These features allow differentiation from
rheumatoid interstitial lung disease which usually is
slow to develop and does not improve dramatically
with therapy.

Some patients require no treatment other than
discontinuation of chrysotherapy. Often patients do
have persistent or severe symptoms that require
administration or glucocorticoids^^ since gold can re-
main in lung tissue for weeks after cessation of ther-
apy.^ With administration of glucocorticoids, im-
provement will occur rapidly in most patients. The
dose of glucocorticoids and duration of therapy is
dependent upon the clinical response of the patient.
It has not been proven, but seems reasonable, that
prompt diagnosis and therapy will lessen the chances
of developing irreversible fibrosis. The syndrome has
been fatal for some patients.

CONCLUSIONS

Gold toxicity must be considered when rheumatoid
arthritis patients develop pulmonary disease. Al-
though uncommon, gold pneumonitis may be fatal
or lead to pulmonary fibrosis if not recognized and
managed promptly. The characteristic features of acute
or subacute pneumonitis occurring in a patient re-
ceiving gold should alert clinicians to the possibility
of the disorder. Aggressive diagnostic pulmonary
procedures to exclude infection or malignancy and
withholding gold therapy will usually allow the di-
agnosis to be established. Treatment with glucocor-
ticoids may be necessary for some patients. ■

REFERENCES

1. Shiel WC, Prete PE: Pleuropulmonary manifestations of rheumatoid ar-
thritis. Semin Arthritis Rheum 1984;13:235-243.

2. Savilahti M: Pulmonary complications following use of gold salts. Ann
Med Intern Fenn 1948;37:263-266.

3. Winterbauer RH, Wilke KR, WheeUs RF: Diffuse pulmonary injury as-
sociated with gold treatment. N Engl J Med 1976;294:919-921 .

4. Evans RB, Ettensohn DB, Fawaz-Estrup F, et al: Gold lung: Recent de-
velopments in pathogenesis, diagnosis and therapy. Semin Arthritis Rheum
1987;16:196-205.

5. Lockie LM, Smith DM: Forty-seven years experience with gold therapy
in 1,019 rheumatoid arthritis patients. Semin Arthritis Rheum 1985;14:238-
246.

6. Kala MH, Van Assendelft AFIW, Ilonen J, et al: Association of different
HLA antigens with various toxic effects of gold salts in rheumatoid
arthritis. Ann Rheum Dis 1986;45:177-182.

7. Davis P, Menard H, Thompson J, et al: One year comparative study of
gold sodium thiomalate and auranofin in the treatment of rheumatoid
arthritis. J Rheumatol 1985;12:60-67.

8. Partanen J, Van Assendelft AHW, Koskimies S, et al: Patients with rheu-
matoid arthritis and gold-induced pneumonitis express two high-risk
major histocompatabUity complex patterns. Chest 1987;92:277-281.

9. McCormick J, Cole S, Lahirir B, et al: Pneumonitis caused by gold salt
therapy: Evidence for the role of cell-mediated immunity in its patho-
genesis. Am Rev Respir Dis 1980;122:145-152.

10. Cooke N, Bamji A: Gold lung. Rheumatol Rehabil 1981;20:129-135.

11. Stuckey BGA, Hanrahan PS, Zilko PJ, et al: HypoganunaglobulLnemia
and lung infiltrates after gold therapy. / Rheumatol 1986;13:468-469.

12. Levinson ML, Lynch JP, Bower JS: Reversal of progressive life threat-
ening gold hypersensitivity pneumonitis by corticosteroids. Am f Med
1981;71:908-912.

13. James DW, Whimster WF, Hamilton EBD: Gold Itmg. BrMed J 1978;1:1523-
1524.

14. Yousem SA, Colby TV, Carrington CB: Lung biopsy in rheumatoid ar-
thritis. Am Rev Respir Dis 1985;131:770-777.

15. Ettensohn DB, Robots NJ, Condemi JJ: Bronchoalveolar lavage in gold
lung. Chest 1984;85:569-570.

16. Scharf J, Nahir M, Kleinhaus U, et al: Diffuse pulmonary injiuy asso-
ciated with gold therapy. JAMA 1977;237:2412-2414.

Drs. Baethge and Wolf are from the Section of Rheumatology, Dept of
Medicine at LSU Medical Center in Shreveport.

Requests for reprints should be sent to Bruce A. Baethge, MD,
LSUMC-S, Box 33932, Shreveport, LA 71130; (318) 674-5930.

JOURNAL VOL 140 FEBRUARY 39

PROFESSIONAL LISTINGS

V !

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THE FERTILITY INSTITUTE OF NEW ORLEANS

(A Professional Corporation)

Richard P. Dickey, MD, PhD

Diplomate, American Board of
Reproductive Medicine
Diplomate, American Board of
Obstetrics and Gynecology

David N. Curole, MD

Diplomate, American Board
of Obstetrics and Gynecology

Phillip H. Rye, MD

Diplomate, American Board
of Obstetrics and Gynecology

Steven N. Taylor, MD

Diplomate, American Board of
Obstetrics and Gynecology

Terry Olar, PhD

Director, InVitro Laboratory
Member, Society for the
Study of Reproduction

REFERRALS ACCEPTED FOR IN VITRO FERTILIZATION
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Elizabeth Messina, RN

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40 JOURNAL VOL 140 FEBRUARY

OF THE LOUISIANA STATE MEDICAL SOCIETY March 1988

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EDITOR

CONWAY S. MAGEE, MD
CHIEF EXECUTIVE OFFICER

DAVE TARVER
GENERAL MANAGER

RENE ABADIE
MANAGING EDITOR

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Chairman

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EMILE K. VENTRE, JR, MD
JAMES W. VILDIBILL, JR, MD
Ex officio

EDITORIAL BOARD

KENNETH B. FARRIS, MD
RODNEY C. JUNG, MD
CONWAY S. MAGEE, MD
W. CHARLES MILLER, MD
ELI SORROW, MD
CLAY A. WAGGENSPACK, JR, MD
WINSTON H. WEESE, MD
PATRICK W. PEAVY, MD

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VOLUME 140 / NUMBER 3 / MARCH

ARTICLES

Schedule of Events for
the 108th Annual
Meeting

Hosea J. Doucet, MD, MPH
Roy A. Berry

Feeding practices of
low^-income infants:

A New Orleans
Health Department Study

Neil H. Baum, MD

Treatment of impotence:
Nonsurgical modalities

Nicholas J. Persich
Edward I. Bluth, MD

Evaluation of
extravasation during
intravenous urography

DEPARTMENTS

Information for Authors

ECG of the Month

Calendar

Otolaryngology /Head

& Neck Surgery Report

Books Received

Classified Advertising

Cover illustration by Eugene New, New Orleans.

INFORMATION FOR AUTHORS

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The JOURNAL welcomes material for publication if submitted by a
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ECG OF THE MONTH

SHORT-CUTS

JORGE I. MARTINEZ-LOPEZ, MD

The 12-lead ECG shown below belongs to a 44-year-old man with documented paroxysms of supraven-
tricular tachycardia. He was on no medications.

What is your diagnosis? Elucidation is on page 6.

JOURNAL VOL 140 MARCH 5

ECG of the Month

Case presentation is on page 5.

DIAGNOSIS — Ventricular preexcitation

The basic rhythm is sinus at 75 times a minute. The
PR interval is extremely short (0.08 sec) and no PR
segment is inscribed. QRS complexes are narrow (0.08
to 0.09 sec) and are associated with non-specific ST
segment and T wave changes in leads 1, 2, AVF, and
V3 through V6. The R waves in the precordial leads
are of large amplitude. There is an early transition
zone of the QRS complexes in the precordial leads.

The combination of short PR interval and narrow
QRS, in a patient who has had paroxysms of supra-
ventricular tachycardia, is consistent with a diagnosis
of a ventricular preexcitation syndrome, and will be
the subject of the discussion to follow.

DISCUSSION

To understand ventricular preexcitation, it is impor-
tant to recall several basic facts. First, the atrioven-
tricular rings and sulci are impenetrable to electrical
impulses originating in either the atria or the ventri-
cles. Second, electrical impulses generated in the sinus
node or atria normally can propagate into the ven-
tricles only by engaging and crossing the AV node
and bundle of His. Third, the AV junctional area is
that portion of the cardiac conducting system re-
sponsible for the delay in the passage of supraven-
tricular impulses into the distal conducting system of
the heart. In the normal heart, therefore, sinus im-
pulses first depolarize the atria and, on their journey
toward the ventricles, are slowed down at the AV
junctional area. Upon exiting from the AV junctional
area, the advancing electrical fronts propagate rapidly
down the bundle of His to both bundle branches,
resulting in near-simultaneous depolarization of both
ventricles. This sequence of events is depicted on the
surface ECG by P-QRS-T cycles. The PR interval,
measured from the onset of the P wave to the first
deflection of the QRS complex, ranges from 0.12 to
0.20 seconds in the adult healthy subject.

Ventricular preexcitation (VPE) is said to be ''pres-
ent when, in relation to the atrial events, the whole
or part of the ventricular myocardium is activated by
the impulse originating in the atrium earlier than

6 JOURNAL VOL 140 MARCH

would be expected if the impulse reached the ven-
tricles by way of the normal specialized conducting
system alone." Based on this definition, it is logical
to conclude that, for VPE to occur, advancing supra-
ventricular impulses must take a "short-cut" to acti-
vate parts or all of the ventricular musculature earlier
than expected. These "short-cuts" are designated as
accessory pathways (AP).

Some APs have been shown to exist, whUe others
are only hypothetical. Among APs considered to be
responsible for VPE are the following: connections
originating in atrial myocardium and inserting in the
corresponding ventricle (bundles of Kent) or origi-
nating in the AV node and inserting in the ventricle
(Paladino tracts); bypass tracts originating in atrial
muscle and inserting in the penetrating bundle of His
(atriofascicular tracts); and connections between the
distal intraventricular conducting system and the ven-
tricle (fasciculoventricular connections or paraspecific
fibers of Mahaim). Still hypothetical are intranodal
bypass tracts and AV nodal malformations that would
eliminate AV junctional conduction delay. Given the
presence of these potential ports of entry into the
ventricular muscle, supraventricular impulses can de-
polarize the ventricles in several ways: entirely by way
of the normal cardiac conducting system; entirely by
way of AP; or over both pathways simultaneously.
The locations and number of existing APs and their
functional status will determine whether or not ECG
findings are present and, when present, their char-
acteristic features.

Recognition of VPE on the surface ECG is achieved
primarily by measurement of the PR interval and the
duration of the QRS complexes and by examining the
QRS configuration. Three major electrocardiographic
patterns are recognized during sinus rhythm. In the-
classic Woljf -Parkinson-White pattern, the PR interval is
short (less than 0.12 sec), the QRS is prolonged (more
than 0.10 sec), a slurred initial deflection of the QRS
is present (delta wave), and the P-J interval is normal.
The pattern of the so-called Lown-Ganong-Levine syn-
drome includes a PR shorter than 0.11 sec and narrow
QRS complexes. The third ECG pattern of VPE is
attributed to the presence of paraspecific fibers of Ma-
haim and consists of a normal PR interval and a QRS
longer than 0.10 sec with a delta wave. Variants of
these three major patterns have been described.

Recognition of VPE is important for two main

reasons. The first is that patients with VPE patterns
are prone to develop tachycardias. Most of the tach-
ycardias observed in patients with VPE are reentrant
and involve the normal conduction system of the heart
and the AP. Less often, paroxysmal atrial fibrillation
or flutter is associated with rapid antegrade conduc-
tion over the AP (innocent bystander tachycardia).
The second reason is that VPE patterns on the ECG
may mimic other cardiac pathologies. Patients with
VPE who develop atrioventricular reentrant tachy-
cardias are said to have VPE syndrome.

In the tracing shown here, the PR interval is so
short (0.08 sec) that the PR segment is not recorded
and the QRS complex is narrow (0.09 sec). The com-
bination of short PR interval and narrow QRS and the
history of recurrent paroxysms of PSVT in this patient
might be construed as favoring the diagnosis of Lown-
Ganong-Levine syndrome. However, close exami-

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nation of the QRS complexes, particularly in leads 2,
AVF, and V3 through V6, discloses the presence of a
small delta wave in those leads. For this reason, it is
more likely that the tracing represents an “incom-
plete" form of Wolf f-Parkinson- White syndrome. This
finding brings into sharp focus one last important
point: it is erroneous to think that the Wolff-Parkin-
son-White syndrome pattern is always associated with
a wide QRS. Because the resulting QRS complexes
during sinus rhythm in patients with bundles of Kent
are fusion complexes, all gradations of fusion can occur
depending on how much of the advancing sinus front
takes a short-cut by way of the AP and how much of
it travels antegrade in the normal conducting system.

■

SELECTED REFERENCES

1. Massumi RA, Vera Z: Patterns and mechanisms of QRS normalization in
patients with Wolff-Parkinson- White syndrome. Am J Cardiol 1971;28:541-
554.

2. Wiener I: Syndromes of Lown-Ganong-Levine and enhanced atrioven-
tricular nodal conduction. Am J Cardiol 1983;52:637-639.

3. Khair Gl, Tristani FE, Barrvrah VS: Dynamic variations in Wolff-Parkinson-
White syndrome: Electrocardiographic and clinical observations. Am Heart
J 1983;105:878-882.

4. Prystowsky EN, Miles WM, Heger }J, et al: Preexcitation syndromes. Med
Clin North Am 1984;68:831-893.

5. Giorgi C, Ackaoui A, Nadeau R, et al: Wolff-Parkinson-White VCG pat-
terns that mimic other cardiac pathologies: A correlative study with the
preexcitation pathway localization. Am Heart J 1986;111:891-902.

Dr. Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

JOURNAL VOL 140 MARCH 7

CALENDAR

April

April 8-10

Louisiana Psychiatric Association/Mississippi Psychiatric
Association Joint Meeting, Natchez, Mississippi. Contact:
Charlene Smith, Louisiana Psyciatric Association, PO Box 15765,
New Orleans, LA 70175; (504)891-1030.

April 9

Selected Topics in Infectious Diseases, Miramar Sheraton
Hotel, Santa Monica, CA. Contact: Beth Hill, UCLA Extension,
PO Box 24901, Los Angeles, CA 90024-0901; (213)825-1901.

April 13-16

Comprehensive Review Course in Hand Surgery, Chicago.
Contact: American Society for Surgery of the Hand, 3025 South
Parker Rd, Suite 65, Aurora, CO 80014; (303)755-4588.

April 13-17

4th Annual Family Medicine Review, Austin, Texas, Con-
tact: Dept of Continuing Medical Education, Scott & White, 2401
South 31st St, Temple, TX 76508; (817)774-2350.

April 14-16

National Cocaine Conference: Clinical Advances in Treat-
ment, Recovery & Relapse Prevention, Orlando, Florida.
Contact: US Training Journal Inc, National Cocaine Conference,
1721 Blount Rd, Suite 1, Pompano Beach, FL 33069;
(800)851-9100.

April 14-17

Controversies in the Management of Skin Tumors, Kiawah
Island Resort, South Carolina. Contact: Plastic Surgery Educa-
tional Foundation, 233 N Michigan Ave, Suite 1900, Chicago, IL
60601, (312)856-1818.

April 16-17

Workshop on Transplantation, Pittsburgh. Contact: American
Society of Anesthesiologists, 515 Busse Hwy, Park Ridge, IL 60068.

April 20-24

Critical Care Medicine 1988: 2nd Annual Review and Up-
date Course, Arlington, VA. Contact: Svetlana Lisanti, Center
for Bio-Medical Communication, 491 Grand Ave, Englewood, NJ
07631; (201)385-1808.

April 22-23

2nd Annual Facial Fracture Surgery, Doubletree Hotel,
Atlanta. Contact: Richard A. Pollock, MD, Georgia Baptist
Medical Center, Box 95, 300 Boulevard NE, Atlanta, GA 30312;
(404)355-9266.

April 22-24

April 23-24

The Cutting Edge 1988/Innovations in Psychotherapy: Help-
ing Individuals and Couples to Change, Hotel Del Cor-
onado, San Diego. Contact: Office of Continuing Medical Educa-
tion, UC San Diego School of Medicine, La Jolla, CA 92093;
(619)534-3940.

April 27-30

Tendon and Soft Tissue Injuries of the Hand, The Cottages
Resort, Hilton Head, South Carolina. Contact: American Society
for Surgery of the Hand, 3025 South Parker Rd, Suite 65, Aurora,
CO 80014; (303)755-4588.

May

May 2-4

NIH Consensus Development Conference: Cochlear Im-
plants, Bethesda, Maryland. Contact: Conference Registrar, Pro-
spect Associates, Suite 500, 1801 Rockville Pike, Rockville, MD
20852; (301)468-MEET.

May 4-6

6th Regions II & III High Blood Pressure Conference/New
Challenges — Creative Solutions, Richmond, Virginia. Con-
tact: Paula A. Ciaverella or Joann T. Richardson, Virginia Dept
of Health, Division of Chronic Disease Control, 109 Governor St,
Madison Bldg, Richmond, VA 23219; (804)786-4065.

May 5-7

May 7

Perspectives in Rheumatology, Century City, CA. Contact:
Beth Hill, UCLA Extension, PO Box 24901, Los Angeles, CA
90024-0901; (213)825-1901.

May 13 - June3

Cruise /Seminar on Risk Management and Comparative
Medicolegal Issues, Hong Kong, China, and Japan. Inter-
national Conferences, Suite C, 189 Lodge Ave, Huntington Sta-
tion, NY 11746; (800)521-0076, (516)549-0869.

8 JOURNAL VOL 140 MARCH

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

LYMPHANGIOMA OF THE NECK
IN INFANTS AND CHILDREN

HENRY A. MENTZ III, MD; HOMER D. GRAHAM III, MD;

PAUL BLAIR, MD

Lymphangiomas are benign congenital lymphatic
malformations found in childhood. There is a
predilection for the head and neck creating
difficult challenges in management decisions.^
Provided is a brief description of the pathogenesis
of this disease and a review of the treatment
options. We present a case report that illustrates a
practical surgical solution in the management of a

life threatening situation.

L ymphangiomas are uncommon benign congenital
lymphatic tumors which present difficult man-
agement decisions. This tumor was originally de-
scribed by Redenbacker in 1828 and by Wernher^ in
1843 as a cystic tumor occurring in certain sites of the
body with predilection for the head and neck. Further
description of these largely cystic tumors over the last
century parallels the description of lymphatic devel-
opment. Furthermore, the terms lymphangioma and
cystic hygroma have been used interchangeably al-
though, from a histological standpoint, lymphan-
gioma is a better term.

ETIOLOGY

There is some controversy regarding the precise etiol-
ogy of this tumor. The most plausible theory was first
presented in 1913 by Dowd.^ It is thought that these
tumors arise from sequestered portions of embryonic
lymph sacs and the accumulation of lymph causes
pressure atrophy and invasion into surrounding
structures.

PRESENTATION

The incidence of this congenital tumor is uncommon.

JOURNAL VOL 140 MARCH 13

A total of 40% of these congenital tumors appear in
the newborn and 80% to 90% have developed by the
second year of life. The appearance of these tumors
beyond puberty is extremely rare. There is a very
slightly increased incidence in males and in occur-
rence on the right. Almost half of these tumors occur
in the head and neck regions. The neck is the single
most common involved structure.

The presentation of this tumor is characteristi-
cally a painless soft swelling or mass in the neck. The
larger lesions may be multilobulated, irregular, com-
pressible, and easUy transLlluminated. Tenderness may
indicate infection. A sudden increase in size may be
due to hemorrhage. Dyspnea and dysphagia indicate
tumor encroachment on respiratory or food passage-
ways.

The differential diagnosis includes branchial cleft
cysts, thyroglossal duct cysts, dermoid cysts, foregut
cysts, rare malignant tumors, deep hemangiomas,
cervical infections, lipomas, and ranulas. The workup
should include a careful history and examination with
special emphasis on the airway and deglutition. En-
doscopic examination can provide valuable insight to
the extent of the tumor. Lymphangiomas can involve
the hypopharynx and larynx. Roentgenograms will
provide little information except that of airway en-
croachment or displacement. Injection of opaque ma-
terial is mentioned only to be discouraged because
cysts do not often communicate and because infec-
tions within these cysts are poorly tolerated. Com-
puted tomographic scans and magnetic resonance im-
aging will provide useful information.

Farber and Landing^ have demonstrated four his-
tologic types: cystic, cavernous, capillary, and he-
mangiolymphangioma types. The cavernous lym-
phangioma is the most frequent and presents the
greatest management problem. Controversy exists in
histologic typing because there is no sharp dividing
line between these four groups. Frequently there is a
combination of these types found in one patient. Fur-
thermore, there is some evidence that there is a change
from capillary to cavernous to cystic type as the dis-
ease progresses.

MANAGEMENT

The treatment goals and principles are universal and
include early treatment, resolution of the entire tu-
mor, the return of function to the involved structures,
the relief of functional complications and emotional
consequences, and a good cosmetic result.^ Manage-
ment options include a wide variety of practices and
procedures. Observation is a dangerous approach be-
cause spontaneous resolution rarely occurs and le-
sions undergo growth and expansion which may lead
to more difficult treatment. Surgeons once favored
aspiration, which rarely resulted in permanent cure.
Complications included infection and hemorrhage
within the cyst leading to further expansion. Aspi-
ration is useful for emergency decompression pre-
ceding surgical cure. A small unilocular cystic lym-
phangioma may respond to palliative treatment such
as aspiration or incision and drainage, but it is oth-
erwise not useful. Various sclerosing agents have in-
cluded morrhuate sodium, boiling water, quinine, ur-
ethan, saturated saline, and 25% glucose. The pitfalls
of sclerosing agents have included damage to adjacent
structures with fibrosis, thickening, and infection.
These may create difficulty in surgical removal often
leading to failure. These agents are rarely used except
in cases of residual tumor left behind. However, in
these cases unroofing of the cysts is a more desirable
alternative.^ Steroids have been used effectively in the
treatment of hemangiomas; however, they have not
proved useful in the treatment of lymphangioma. Ir-
radiation, advocated in the past, provided occasional
cures, but failures were common. Also, irradiation
produced damage to other structures with potential
induction of malignancies, potential for local growth
retardation, cosmetic deformity, infection, and death.

Surgery has been deemed the treatment of choice
for lymphangioma. A primary concern in manage-
ment must be constant maintenance of a patent air-
way: tracheostomy may be necessary in this case.
Other considerations include deglutition and nerve
function. Most authors recommend complete excision
if possible. Vital structures should be preserved even
at the expense of incomplete excision. The most dif-
ficult head and neck tumors involve the eyelids, max-
illa, and mandible. In these areas, many times, the
tumors are removed in staged procedures. When gross

14 JOURNAL VOL 140 MARCH

tumor was completely excised the recurrence rate was
in the area of 30% and when incompletely excised the
recurrence rate exceeded 70%.^ Any residual lym-
phangioma is susceptible to infection and recurrence.
The unroofing of residual cysts may potentiate the
cure. These patients must have vigorous preoperative
treatment of oral infection and preparation of the skin.
Antibiotics should be used when infection is present
and prophy tactically during the perioperative period.
Surgical drains and pressure dressing should be used
to eliminate potential spaces. Surgical complications
have included muscle weakness, Horner's syndrome,
recurrent laryngeal nerve paralysis, post-operative in-
fection, recurrence, airway obstruction, and death.

CASE STUDY

An 11-day-old black female was noted to have a small
sublingual lesion on incidental exam. Four months
later, she developed a tender enlarging submaxillary
mass, which was fluctuant and erythematous, and
she was treated with parenteral antibiotics and hos-
pitalization. Eventually she was referred to the Tulane
Department of Otolaryngology with the diagnosis of
lymphangioma. She then developed inspiratory stri-
dor and dysphagia. At six months of age she was
taken to surgery for excision of this enlarging mass.
Treatment required tracheotomy and bilateral modi-
fied radical neck and supramyelohyoid dissections.
Some residual tumor remained within the lingual
musculature. At both two months and one year later
she required laser excision of hypopharyngeal lym-
phangioma. She is now being followed in our clinic
with recurrent tumor in the hypopharynx, tongue,
and lower one-third of the face, and she will require
reexcision and repeat laryngoscopy.

CONCLUSION

Lymphangioma is a benign congenital lymphatic mal-
formation which presents difficult management de-
cisions. In a most serious situation, lymphangioma in
the neck can cause life threatening airway compro-
mise and deglutition difficulty and must be treated
with urgency. Radical surgery preserving function and
anatomic structure has been the treatment of choice
in most patients. ■

REFERENCES

1. Saigo M, Munro IR, Mancer K: Lymphangioma: A long term followup
study. Blast Reconstr Surg 1975;56:642-651.

2. Wemher A: Die Angeborenen Zysten-Hygrome und die inhen verwandten
Geschwulste in anatomisher diagnostischer und thrapeutischer Beziehung. Gies-
sen, GF Heyer, 1843:p76.

3. Dowd CN: Hygroma cysticum coUi: Its structure and etiology. Ann Surg
1913;58:112-132.

4. Landing BH, Farber S: Atlas of Tumor Pathology. Washington, DC, Armed
Forces Institute of Pathology, 1956, Sec III, fasc 7.

5. Cohen S, Thompson J: A survey of pediatric lymphangioma. Ann Otol
Rhinol Laryngol [Suppl] 1987;l-20.

6. Briggs D, Leix F, Snyder WH, et al: Cystic and cavernous lymphangioma.
West } Surg 1953;61:499-506.

Drs Mentz, Graham, and Blair are from the Dept of Otolaryngology-
Head & Neck Surgery at Tulane Medical School in New Orleans.

Reprint requests should be sent to Paul A. Blair, MD, Dept of
Otolaryngology-Head & Neck Surgery, Tulane Medical School, 1430
Tulane Ave, New Orleans, LA 70112.

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April 9-10, 1988

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JOURNAL VOL 140 MARCH 15

FEEDING PRACTICES OF
LOW-INCOME INFANTS:

A NEW ORLEANS HEALTH DEPARTMENT STUDY

HOSEA J. DOUCET, MD, MPH; ROY A. BERRY

16 JOURNAL VOL 140 MARCH

A survey of infants from birth to 1 year of age was
conducted at city-operated Child Health Centers to
determine the infant feeding practices and
attitudes toward nutrition of needy participants of
federal nutrition programs. It was determined that
in this largely black population, 88% of the infants
were bottle-fed, 27% had cereal introduced by age
1 month, and many were already on cola drinks.
Most participants recalled receiving information on
breast- or bottle-feeding but few recalled receiving
information on the introduction of foods other
than milk. Most parents (76%) desired more
information on the subject. Participants in these
programs were clearly not practicing the current
recommended guidelines on infant nutrition with
regard to introduction of foods other than milk.
The nutrition education efforts in public health
clinics should emphasize more teaching on the
appropriate timing for introduction of foods other
than milk into the diet of infants, especially since
parents have expressed an interest in this area.

I NFANT FEEDING PRACTICES in the period from birth
through one year vary greatly among different pop-
ulation groups in this country and throughout the
world. For centuries, human breast milk was the only
available source of nutrition for infants during the first
few months of life. Since the introduction of com-
mercial infant formulas in the 30s and 40s, breast-
feeding has declined in the United States reaching a
low point of 22% to 25% in the early 70s.^ Breast-
feeding then began an upward trend which has con-
tinued until the present. The national incidence of
infants breast-feeding in the hospital was reported to
be as high as 58% in 1981.^ The rate of increase of
breast-feeding has been slower in the less educated
and lower socioeconomic groups which continue to
have relatively low levels of breast-feedings.^ Infants
are also receiving supplemental foods other than breast
irdlk or formula at an early age.^ The American Acad-
emy of Pediatrics (AAP) and other professional or-
ganizations recommend breast-feeding as almost al-
ways preferable to commercial formulas, and they
also recommend that foods other than breast milk or
formula not be introduced prior to the age of four to
six months, at which time the addition of iron en-
riched foods is encouraged.^' ^

This study was undertaken to determine infant

feeding practices and attitudes toward nutrition among
federal nutrition program participants attending Child
Health Centers (previously called Well Baby Clinics)
operated by the New Orleans Health Department.
Determination of this more precise information can
facilitate the nutrition education component of these
programs.

METHODS

During the summer of 1984, 409 adults accompanying
infants from birth through 1 year were interviewed
at six of the eight Child Health Centers operated by
the New Orleans Health Department. At these cen-
ters patients receive routine immunizations, physical
examinations, growth and development determina-
tions, and screenings for anemia, lead poisoning, vi-
sion, and hearing problems. In addition they may be
eligible to receive nutritional counseling and certifi-
cation in either of two federal nutritional programs:
Women, Infant and Children (WIC) or Commodity
Supplemental Food Program (CSFP). To qualify for
these programs, an infant had to meet residential re-
quirements (Orleans Parish), financial requirements
(145% to 185% of poverty level), and nutritional cri-
teria established by the US Department of Agricul-
ture. The CSFP provides monthly food packages of
infant formula and/or food supplements to families.
The WIC Program provides a series of vouchers which
can be used at participating food stores to purchase
designated foods and infant formula. These programs
target the low income, high risk population of chil-
dren from birth to 6 years of age. Orleans Parish has
a total participation of approximately 4,500 infants on
the WIC program and 22,000 infants and family mem-
bers on the CSFP. This does not include participation
in the Elderly CSFP.

During the interviews, three students of the Tu-
lane School of Public Health and Tropical Medicine
administered a standardized questionnaire according
to set criteria. The questionnaire was read to individ-
ual adults accompanying infants in the clinic waiting
rooms. All persons interviewed were participants in
one of the two food programs. Individuals not par-
ticipating in either program were excluded from the
study. The questionnaire was devised to answer ques-
tions regarding the incidence of breast-and formula-
feeding, the timing of the introduction of other foods,

JOURNAL VOL 140 MARCH 17

Fig 1. TIMING OF INTRODUCTION OF NON-MILK FOODS INTO THE DIET
OF INFANTS BY 1 MONTH AND 3 MONTHS OF AGE

AGE ONE MONTH I I AGE THREE MONTHS [

food preparation techniques,
and the sources of information
upon which feeding decisions
were based. Each interview
lasted approximately 30 min-
utes.

RESULTS

The majority of infants in this
study were black (89%) with
the remainder racially divided
among Asian, Hispanic, and
white populations. The aver-
age infant's age was 5 months
and the average maternal age
was 24 years. Prenatal care for
most participants had been
provided by Charity Hospital
of New Orleans (61%). No sig-
nificant differences in the re-
sults from the six different clinic
sites were noted.

The most common method
of infant feeding was deter-
mined to be bottle-feeding
(88%). Only 7% of infants were
breast-fed exclusively, and 5% of infants were both
breast-and bottle-fed. Among the bottle-feeders, 58%
considered breast-feeding or a combination of breast-
and bottle-feeding to be healthier than bottle-feeding
only. Most attendants stated that they chose bottle-
feeding because it was "easier" (41%) or stated that
they had never considered breast-feeding (31%); only
7% gave medical reasons or a physician's recommen-
dation as the reason for choosing that method. Of the
participants currently bottle-feeding, only 20% had
previously breast-fed the child they accompanied to
the clinic or had breast-fed an earlier child; 80% had
never attempted breast-feeding.

Participants were asked when supplemental foods
other than milk or formula were first introduced into
their infants' diet. Many had already done so by age
1 month (Fig 1). A total of 27% of these infants had
cereal introduced by the age of 1 month or earlier.
Several infants had foods other than milk introduced
during the first week of life. By the age of 3 months,
54% of the 409 infants had been introduced to cereal.

39% had received fruits or fruit juices, 24% had re-
ceived vegetables, and 9% had received meats. Many
participants were currently giving cola drinks (17%)
or Kool-Aid® mixtures (18%) to their infants. Of the
participants, 33% admitted to regularly adding sugar
or syrup to their infants' drinking water.

The majority of participants indicated that infor-
mation on infant feeding had been provided by a
physician or a nurse (Table 1). However, more of
these participants remembered receiving information
on breast-and bottle-feeding than remembered re-
ceiving information on the introduction of other sup-
plemental foods. A total of 35% stated that they re-
ceived no information on the introduction of foods
other than milk. A smaller number stated that they
had received no information on breast- (19%) or bot-
tle-feeding (21%). A total of 76% wanted more infor-
mation on the introduction of supplemental foods;
54% wanted more information on bottle-feeding; only
38% stated that they wanted additional information
on breast-feeding.

18 JOURNAL VOL 140 MARCH

DISCUSSION

Prior to this century, the most important food avail-
able to an infant during the first months of life was
human breast milk. During these first few months,
cow's milk, which has a high osmolarity and an excess
renal excretory load of protein and minerals, is poorly
tolerated by human infants. An infant could not in-
gest "adult" or solid foods until about the age of six
months when he could chew, swallow, and exhibit
good head control. Therefore, it was several months
before other foods could be added to his diet.

Today, however, a wide variety of food is avail-
able to an infant during his first year. Most commer-
cial formulas are modified from a cow's milk base with
levels of protein and ash decreased to levels near those
of human milk.^ Other milks or milk substitutes are
available for infants who cannot tolerate cow's milk,
and as more is learned about infant physiology, prep-
arations are improved accordingly. With current
methods of grinding, straining, and preserving, foods
which were once only "adult" foods are now available
as baby foods, eg, spinach, turkey, beef. These baby
foods can be ingested at very early ages, even during
the first weeks of life.

These changes are not without consequences,
however, and do not mean that cow's milk and other
foods are satisfactory replacements for the once tra-
ditional mainstay of mankind — human breast milk.
The AAP has recommended that "breast milk is al-
most always preferred to formula."^ Reasons often
cited include the association of breast-feeding with
fewer infections, fewer allergic problems, optimum
nutrition during growth, and improved psychological
and intelligence levels.^

Based on this study, it appears that current rec-
ommendations on infant feeding practices during the
first year of life are not being adequately followed in
our population. Most mothers in this study were not
breast-feeding, although most of those interviewed
felt that breast-feeding would be better for their in-
fant. Unfortunately, they had decided to bottle-feed
in spite of this. Furthermore, 60% did not desire any
more information on the subject of breast-feeding.

Other studies have stated multiple reasons why
mothers do not breast-feed.^ Many mothers consider
breast-feeding inconvenient for a modern lifestyle,
find it embarrassing, or have a fear of inadequate

TABLE 1

SOURCES OF INFORMATION ON INFANT FEEDING

Source Breast Bottle Other Foods

Physician

26%

24%

16%

Nurse

60%

37%

Friend

Relative

No one

19%

21%

35%

Others

lactation, infection, or cosmetic after-effects of breast-
feeding. The knowledge of breast-feeding that was
traditionally passed from mother to daughter has also
largely been lost.

It has been reported by other investigators that
the decision on the method of feeding was made be-
fore pregnancy by 60% of mothers who breast-fed and
40% of mothers who bottle-fed.^ Very few mothers in
this study reported waiting until after delivery to de-
cide to breast-feed (10%) or bottle-feed (20%). This is
confirmed in our study by the small number of our
participants requesting more information on breast-
or bottle-feeding at the time of their visits to the Child
Health Centers. Due to the large majority of mothers
bottle-feeding today, there is little incentive for a
mother to make the decision to breast-feed at the time
of delivery. There is even less incentive for a low-
income mother to decide to change feeding methods
once she attends a well baby clinic, and bottle-feeding
has become well established. Therefore, a more ef-
fective time to promote breast-feeding is prior to an
infant's delivery. In this manner, mothers can ade-
quately prepare for breast-feeding and the misinfor-
mation previously stated can be corrected. As noted,
most mothers attending the Child Health Centers were
not interested in further information on breast-feed-
ing or bottle-feeding.

Concerning the introduction of supplemental
foods, the majority of infants in this study had foods
other than milk introduced by the age of 3 months,
and over one quarter had started cereal by the age of
1 month. While these figures were not quantified, and
we cannot assess their fuU impact, this information

JOURNAL VOL 140 MARCH 19

indicates serious variations from professional rec-
ommendations. The participants of this study appar-
ently recognized their ignorance on when to intro-
duce foods other than milk, and over three fourths
wanted more information on this subject.

Reasons often cited for the early introduction of
supplemental foods include a desire of mothers to see
their infants gain weight rapidly, social pressure to
conform to how other (often older) children were fed,
effective marketing by the infant food industry, and
the belief that the feeding of solid food will help an
infant to sleep. None of these reasons has any nutri-
tional advantage, and each should be countered in
any educational program. The early introduction of
supplemental foods can have widespread and pos-
sibly harmful effects which include development of
diarrhea, food and/or other allergies, obesity, and poor
nutritional habits.®

Prior to the age of 4 to 6 months, an infant lacks
the neuromuscular control of the head and neck nec-
essary for chewing and swallowing foods as well as
the ability to indicate a desire for more or less food.
Also, in the first few months of life, the intestinal tract
and kidneys have not developed the proper mech-
anisms for coping with foreign proteins and electro-
lytes, but are designed to digest the proteins, lipids,
and carbohydrates found in breast milk. The AAP
recommends that:

At about four to six months of age, a variety
of foods should be introduced one at a time, at
intervals of a week or more. The sequence of
foods is not critical, but iron-fortified, single-
grain infant cereals are a good early choice. The
addition of individual (not mixed) vegetables,
fruits, or meats introduces a variety of foods and
sets the pattern for a diversified diet.^

and many of these infants were currently on cola or
Kool-Aid® drinks. There is an equal need for educa-
tion on breast-feeding in this population, but the most
appropriate and most effective time for this education
is prior to attendance at well baby clinics. ■

REFERENCES

1. Hendershot GE: Domestic review, trends in breast-feeding. Pediatrics
1984;74(supp):591-602.

2. American Academy of Pediatrics: On the Feeding of Supplemental Foods
to Infants. Pediatrics 1980;65:1178-1181.

3. Foman SJ: What are infants fed in the United States? Pediatrics 1975;56:350-
354.

4. American Academy of Pediatrics: Breast-feeding. Pediatrics 1978;62:591-
601.

5. Miller SA, Chopra JG: Problems with human milk and infant formulas.
Pediatrics 1984;74(supp):639-647.

6. Simopoulos AP, Grave GD: Factors associated with the choice and du-
ration of infant-feeding practice. Pediatrics 1984;74(supp):603-614.

7. Sacks SH, Brada M, Hill AM, et al: To breast feed or not to breast feed.
Practitioner 1965;216:183-191.

8. Leberthal E: Impact of digestion and absorption in the weaning period
on infant feeding pracHces. Pediatrics 1985;75(supp):207-215.

Dr Doucet is the Chief of Clinical Services/Communicable Diseases of
the New Orleans Health Department and Associate Professor of
Pediatrics at Tulane University School of Medicine in New Orleans.

Mr Berry was a senior medical student at Tulane University School of
Medicine and a candidate for the combined MD/MPH degree. He has
since graduated and is currently an intern in internal medicine at the
University of California at Davis in Sacramento, California.

Reprint requests should be sent to Hosea }. Doucet, MD, MPH,
Associate Professor of Pediatrics, Tulane University School of Medicine,
Dept of Pediatrics, 1430 Tulane Ave, New Orleans, LA 70112.

CONCLUSION

In this population of low-income mothers and infants,
there is apparently a great need and desire for edu-
cation on how to introduce foods other than breast
milk or formula. Participants in this study were in-
troducing supplemental foods at too early an age but
were desirous of more information. Over one fourth
of the infants had cereal introduced before 1 month
of age, over one half had cereal added before 3 months.

20 JOURNAL VOL 140 MARCH

TREATMENT OF IMPOTENCE

NONSURGICAL MODALITIES

NEIL H. BAUM, MD

Impotence may result from a primary disorder of
the male reproductive system or, more commonly,
from physical or psychogenic disturbances. Recent
advances in the pathophysiology of the erection
mechanism has led to the development of
nonsurgical treatment of this common sexual
dysfunction. This is the first of a two-part series.
A future article discusses the surgical approach to

impotence.

M en have historically looked for the pill, injec-
tion, or magic potion that could restore their
youth and potency without surgery and without side
effects. Unfortunately, the ideal nonsurgical treat-
ment has not been discovered. However, great ad-
vances in this common medical problem that affects
nearly 10 million American men have taken place in
the last few years. This paper will review some of the
latest nonsurgical treatments.

NO TREATMENT

It is not unusual for a man to learn that his erectile
failure is on a physical basis and accept the diagnosis
without any further workup or treatment. Often-
times, the partner of an impotent man has a conscious
or subconscious question of infidelity. In this situa-
tion, the man wants to convince his partner that there
is no loss of love or affection and that no third party
is involved. If the physician recognizes this set of
circumstances, he can be very helpful in alleviating a
great source of anxiety and tension by reassuring the
man's partner that the impotence is on an organic or
physical basis and that there is no loss of love or
affection. ^

JOURNAL VOL 140 MARCH 27

HORMONE REPLACEMENT

PROLACTIN

The subject of androgen replacement for erectile dys-
function is an area of considerable controversy. It is
well documented that the serum testosterone level
declines only minimally with age. The total serum
testosterone level usually remains within a normal
range until age 70. Several studies have shown that
the serum testosterone level is not lower in impotent
men than in potent men.^'^ It is also well accepted
that serum testosterone is more responsible for main-
taining the libido or sex drive than for obtaining or
maintaining an erection. Recently more information
regarding the pathophysiology of the hypothalamic-
pituitary-testicular axis has become available and more
cases of endocrinologic impotence are being discov-
ered. It is important that all impotent patients have
a screening serum testosterone level. Low-normal or
decreased levels require a more thorough endocrine
evaluation.

Patients with documented decreased testoster-
one levels usually have an excellent response to an-
drogen replacement. Intramuscular injections of a long
acting testosterone supplement such as testosterone
enanthate produce a dose-related increase in the li-
bido as well as in frequency and quality of erections.
The intramuscular route is preferred to oral admin-
istration because of the variable absorption from the
gastrointestinal tract and the association of cholestatic
jaundice with oral testosterone. It is important that
aU patients receiving long-term androgen therapy have
periodic liver function tests. All patients over age 50
require frequent rectal examinations and measure-
ments of serum acid phosphatase since exogenous
androgens can activate a carcinoma of the prostate.
There are no clear cut guidelines for the use of an-
drogens in the impotent patient with a normal serum
testosterone and no obvious organic pathology. I think
that a “short course" of androgen therapy often is
beneficial and is associated with negligible morbidity.
The general improvement in well-being and sexual
performance is most likely related to either the ana-
bolic effects of the androgen or the expectation of
improvement associated with the physician's confi-
dence that the problem is amenable to treatment rather
than to any specific endocrine action on potency.

Recently there has been an increased awareness of
the association of the role of prolactin and impotence.
One study reported 19% of impotent patients referred
for medical evaluation were found to have hypotha-
lamic-pituitary disease. Nearly one-quarter of these
patients had prolactin secreting tumors.^ Although
this statistic seems high, it is important to rule out
this treatable cause of impotence. Most patients with
prolactin secreting tumors are impotent and in nearly
half of these patients, the chief complaint is impo-
tence. Most patients will have a low-normal or slightly
decreased serum testosterone level. The diagnosis is
confirmed by elevated levels of prolactin. The finding
of hyperprolactinemia warrants a complete pituitary
evaluation. The treatment of impotence associated
with hyperprolactinemia has been successful with the
use of the long-acting dopamine receptor agonist
bromocriptine mesylate. This drug decreases the el-
evated prolactin and consequently raises the testos-
terone level with improvement in libido and potency.

DRUG-ASSOCIATED IMPOTENCE

The list of medications associated with sexual im-
pairment is lengthy.'^ The most common categories
include antihypertensives, sedatives, tranquilizers,
analgesics, antiandrogens, anticholinergics, and drugs
with abuse potential. I believe patients should be in-
formed about the sexual side effects of these drugs;
however, the likelihood of this complication should
be minimized, otherwise patients can conveniently
"develop" impotence as a result of the self-fulfilling
prophecy generated by a well-meaning physician. It
is also important to stress to the patient that if a sexual
dysfunction occurs, they should report the problem
rather than discontinue the medication. Oftentimes
the sexual side effects of medication can be reversed
by decreasing the dose or changing to another class
of drug that accomplishes the same goal but without
producing erectile dysfunction.

INTRACORPORAL INJECTION

Self-injection of vasodilating drugs into the penis has
been a new nonsurgical modality for treating organic
impotence. Several drugs have been tried but the most
successful is a combination of papaverine hydrochlo-

28 JOURNAL VOL 140 MARCH

ride and phentolamine mesylate.^ This has been an
effective treatment regardless of the age of the patient
or the etiology of the erectile dysfunction. The patient
usually obtains an erection in five to ten minutes after
injection into one of the corporal bodies of the penis.
The erection usually lasts 30 to 45 minutes. Compli-
cations are rare and consist of ecchymosis at the in-
jection site, corporal fibrosis if the same injection site
is used repeatedly, and prolonged erection which can
be reversed by aspiration/irrigation with epineph-
rine.^ I recommend that patients do not use intracor-
poral injections more frequently than once a week.
The Food and Drug Administration has not approved
or disapproved the use of papaverine hydrochloride/
phentolamine mesylate for intracorporal injections.
Consequently, I request that the patients sign a spe-
cial informed consent form and that they watch a
video tape on sterile technique. The use of intracor-
poral injections has been an accepted modality for
many patients with organic impotence who do not
wish to have surgery or who cannot afford surgery.

ALPHA-ADRENERGIC ANTAGONIST

Recently the role of catecholamines and their con-
tribution to the physiology of erections has been de-
scribed. Yohimbine is an alpha adrenergic blocking
agent derived from the bark of an African tree. This
drug has been demonstrated to be successful in the
management of “selected cases" of organic impo-
tence.^ The drug is well tolerated with only occasional
nausea and dizziness that subsides when the dosage
is decreased and then increased by small increments.

GADGETS

There are a number of devices that patients can pur-
chase over-the-counter that can "create an erection."
Most of these devices work on the principle of placing
a stiff silicone condom over the penis then applying
negative pressure to increase the blood supply into
the vascular chambers of the penis. With an increase
in the blood supply the penis becomes rigid and a
rubber band or tourniquet is applied at the base of
the penis to trap the blood within the penis. These
devices are somewhat cumbersome to use and their
use can be complicated by ecchymoses and priapism
if the tourniquet is left in place too long.

SEX THERAPY

The most successful treatment of psychogenic im-
potence is sex therapy. It is important that the patient
and his partner be referred to a qualified sex therapist,
a psychologist, or a psychiatrist who has an interest
and expertise in the management of sexual dysfunc-
tions. The highest success rate in the treatment of
impotence by sex therapy is in the patient who: 1)
has had impotence less than one year, 2) has a stable
relationship with his partner, 3) has motivation to
enter sex therapy, and 4) has a partner willing to
participate with him in treatment.

SUMMARY

Male sexual dysfunction is a concern that is quite
prevalent in our society. Until recently the only treat-
ment for impotence was sex therapy and penile
prostheses. Now, with greater understanding of the
pathophysiology of the erection mechanism, effective
new nonsurgical treatment is available. ■

REFERENCES

1. Federman DD: The assessment of organic function: The testis. N Engl J
Med 1971;285:901.

2. Smith KD: Rapid oscillations in plasma levels of testosterone, lutenizing
hormone, and follicle-stimulating hormone in men. Fertil Steril 1974;25:965.

3. Spark RF: Neuroendocrinology and impotence. Ann Intern Med 1983;98:103.

4. Van Arsdalen K, Wein A: Drug-induced sexual dysfunction in older men.
Geriatrics 1984;39:63.

5. Zorgniotti A, Lefleur R: Autoinjection of the corpus cavemosum with a
vasoactive drug combination for vasculogenic impotence. / Urol 1985;133:39-
41.

6. Padma-Nathan H, Goldstein 1, Krane R: Treatment of prolonged or pria-
pistic erections following intracavernosal papaverine therapy. Semin Urol
1986;4:236-238.

7. Morales A, Surridge HC, Marshall PG, et al: Nonhormonal pharmacol-
ogical treatment of organic impotence. / Urol 1982;128:45-47.

Dr Baum is a urologist affiliated with Touro Infirmary in

New Orleans.

Reprint requests should be sent to Dr Baum at 3525 Prytania St,
Suite 614, New Orleans, LA 70115.

JOURNAL VOL 140 MARCH 29

PHYSICIANS^
SCHEDULE
SOME TIME FOR
YOUR COUNTRY.

Discuss the opportunities
with our Army Medical Person-
nel Counselor.

FOR

SURGEONS
LOOKING FOR
ACHAUENGE.

Your challenge could be the
Army Reserve unit near you. It's a
unit that requires the services of
surgeons.

You’ll also have an opportunity
to participate in a number of pro-
grams in which you’ll be able to
exchange views and information with
other surgeons from all over the
country.

To find out about the benefits of
serving with a nearby Army Reserve
unit, we recommend you call our
Army Medical Personnel Counselor.

PHYSICIANS.THERE
ARE TWO KINDS
OF FLEXIBILITY IN
THE ARMY RESERVE
WE THINK YOU'LL LIKE.

Tw, the opportunity to
explore other phases of medi-
cine, to add a different kind of
knowledge— the challenge of
military health care. It’s a flexi-
bility which could prove to be
both stimulating and reward-
ing, with the opportunity to
participate in a variety of
programs that can put you in
contact with medical leaders
from all over the country.

See how flexible we can
be, call our Army Medical
Personnel Counselor.

ARMY RESERVE.
BEALLYOUCANBE.

HERE'S ONE DOCTOR
WHO WON'T PAY
HIS MALPRACTICE
PREMIUMS THIS YEAR.

The Army covers his premiums.
Since he’s an Army Physician, there are
a lot of worries associated with private
practice that he won’t have to contend
with. Like excessive paperwork, and the
overhead costs incurred in running a
private practice.

What he will get is a highly challeng-
ing, highly rewardingexperience. The
Armyoffersvaried assignments,
chances to specialize, or further your
education, and to work with a team of
dedicated health care professionals.

Plus a generous benefits package.

If you’re interested in practicinghigh
quality health care with a minimum of
administrative burdens, examine Army
medicine. Talk toyourlocal Army
Medical Department Counselor for
more information.

ARMY MEDICINE.
BEAUYOUCANBE.

MAJOR OPPORTUNITIES FOR
HEALTH PROFESSIONALS.

Army/Army Reserve Medicine
144 Elk Place, Suite 1514
New Orleans, LA 701 12
Call collect; (504) 589-2373

EVALUATION OF EXTRAVASATION
DURING INTRAVENOUS UROGRAPHY

NICHOLAS J. PERSICH; EDWARD I. BLUTH, MD

Extravasation during intravenous pyelography can
be an ominous sign indicating frank pelvic or
ureteral rupture; however, it can also indicate a
forniceal tear which is a benign complication. The
authors present a case and discuss the
differentiation between true rupture of the upper
collecting system and forniceal extravasation in an

obstructed system.

I N A PATIENT who complained of left flank pain, in-
travenous pyelography with abdominal compres-
sion showed extravasation of contrast from the left
kidney into the retroperitoneal space. Extravasation
of urine usually occurs from rupture of a calyceal for-
nix as a result of obstruction. The primary cause ap-
pears to be a rapid rise in intrapelvic pressure with
rupture of the fornix acting as a physiologic release
mechanism to decrease the intrapelvic pressure. This
process is usually benign but must be differentiated
from frank pelvic or ureteral rupture which requires
surgical intervention.

CASE REPORT

A 32-year-old man was seen in the emergency room
with left flank pain. Physical examination revealed
left costovertebral angle tenderness and hematuria.

An intravenous pyelogram with compression was
performed. Scout films revealed several calcific dens-
ities in the left kidney and a 5 mm calculus superior
to the left L-3 transverse process and lying in the
apparent pathway of the left ureter. Following injec-
tion of contrast media, there was delayed excretion ►

JOURNAL VOL 140 MARCH 35

Fig 1. 90-minute deiayed iVP film demonstrating
left hydronephrosis. In addition, consider-
able extravasation of contrast is seen sur-
rounding the pelvocalyceai system and
proximal left ureter.

from the left kidney with dilatation of the upper col-
lecting system. Slight extravasation from the renal
sinus and hilum of the left kidney was noted on the
10-minute film with subsequent extension down the
lateral border of the psoas muscle. Further extrava-
sation was noted on the 90-minute film (Fig 1). Con-
trast media had flowed down the fascial planes around
the left ureter. Two days following the examination,
the patient underwent extracorporeal shock wave
lithotripsy after the ureteral stone was displaced into
the kidney. The renal calculus was fragmented and
all the stone fragments passed easily. The patient left
the hospital the next day without evidence of left renal
calculi.

36 JOURNAL VOL 140 MARCH

DISCUSSION

In evaluating extravasation during intravenous urog-
raphy, it is important to determine the site of leakage
of the contrast media. There has been some confusion
in the past as to the distinction between a true rupture
of the upper collecting system and forniceal extra-
vasation in an obstructed system. In a previously un-
damaged collecting system, when there is an increase
in intraluminal pressure, especially if it is acute, the
point of extravasation is at the weakest point in the
system — the calyceal fornix.^ The elevated pressure
in obstruction can cause a minute forniceal tear with
urine or contrast media leaking into the renal sinus
and then dissecting down around the ureter. The for-
niceal site of extravasation is felt to be a normal safety
valve for alleviation of increased pressure.^ This phys-
iologic decompression of the acutely obstructed sys-
tem is not uncommon.^ How often forniceal extra-
vasation does occur in urography depends usually on
three factors — the amount of contrast medium used,
whether abdominal compression is applied, and the
degree of obstruction. The incidence of extravasation
was shown to increase as the bolus of contrast that
was used was increased, when abdominal compres-
sion was used, and when the collecting system was
completely obstructed.^ Patients rarely become symp-
tomatic from forniceal extravasation. When symp-
toms do occur, they are usually the result of leakage
of infected urine and formation of an abscess.^

In contrast to forniceal extravasation, true rup-
ture of the renal pelvis or ureter is totally non-
physiologic. Trauma is the most common cause with
calculus disease the next most common. Rupture has
also been reported in a previously damaged collecting
system secondary to previous kidney surgery, recent
instrumentation (ureteric catheterization or retro-
grade pyelography), infection, or neoplasm.^ The
mechanism by which a calculus causes rupture is either
from necrosis of the wall around the stone or from a
tear formed during the passage of the stone. When
the calculus obstructs distally in the ureter, the ele-
vated pressure that is produced can cause the dam-
aged wall to rupture or it can increase the size of the
original tear with subsequent rupture and extrava-
sation.^ Symptoms from frank rupture of the pelvis
or ureter are usually severe, and often medical and
surgical intervention are indicated. How aggressive

treatment should be is based on the requirements
imposed by the patient's clinical condition, the per-
sistence of obstruction or extravasation, or the pres-
ence of a complication such as urinoma or abscess.®
Further differentiation between these two entities
may be aided by certain observations of the roent-
genogram. The first is to look specifically for contrast
material around a calyx, the presence of which clearly
points to forniceal rupture. Secondly, demonstration
of the ureter seems to be a helpful point in differ-
entiation. In cases showing tears or rupture of the
pelvis, the ureter on the affected side was never or
only occasionally visualized, while in cases with for-
niceal extravasation a typical "pipe" ureter was pres-
ent. And further, re-examination 24 to 48 hours after
the initial examination will show, in most cases of
forniceal rupture, disappearance of the extravasation,
whereas in cases of pelvic or ureteral rupture, the
roentgenologic appearance remains unchanged. These
conditions are not without exception. Clinically, also,
there is a difference between forniceal and pelvic rup-
ture. Patients who experience actual rupture of the
pelvis or ureter tend to have a higher temperature,
to appear more ill, and to have an increased white
blood cell count. ^

In this case, the pyelographic appearance and the
stable clinical condition of the patient are consistent
with forniceal rupture as the cause of extravasation.
Furthermore, the patient had no past history of
trauma, instrumentation, or kidney disease. There was
also no worsening of symptoms following urography,
making it unlikely that frank pelvic or ureteral rupture
had occurred. The importance of recognizing this type
of extravasation as a benign complication of acute
obstruction and distinguishing it from renal rupture
following trauma cannot be overemphasized. Failure
to understand this association may lead to unwar-
ranted surgical exploration. ■

REFERENCES

1. Orkin LA: Spontaneous nontraumatic extravasation from ureter. / Urol
1952;67:272-283.

2. Khan AU, Malek RS: Spontaneous urinary extravasation. / Urol 1976;116:161-
165.

3. Schwartz A, Caine M, Hermann G, et al: Spontaneous renal extravasation
during intravenous pyelography. Am ] Radiol 1966;98:27-39.

4. Bemadino ME, McClennan BL: High dose urography: Incidence and re-
lationship to spontaneous peripelvic extravasation. Am J Radiol 1976;127:373-
376.

5. Hadar H, Giro S: Spontaneous extravasation of urine in chronic ureteric
obstruction. Urology 1979;14:30-32.

6. Jeppesen FB: Spontaneous rupture of kidney. / Urol 1961;86:489-492.

7. Borkowski A, Canpliczka M: Nontraumatic extravasation from the ureter.
Int Urol Nephrol 1974;5:271-275.

8. Abeshouse BS: Rupture of the kidney pelvis. Surg Gynecol Obstet 1935;60:710-
729.

9. Narath PA: Extrarenal extravasation obstruction in the course of intra-
venous pyelography. / Urol 1978;39:65-75.

Mr Persich was a fourth year medical student at LSU School of
Medicine. He has since graduated and is currently an intern at Charity

Hospital in New Orleans.

Dr Bluth is from the Dept of Radiology at Ochsner Clinic and Alton
Ochsner Medical Foundation in New Orleans.

Reprint requests should be sent to Dr Bluth, Ochsner Clinic,
1514 Jefferson Hwy, New Orleans, LA 70121.

nicius

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JOURNAL VOL 140 MARCH 37

Physicians Recognition Award

Seventeen physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
December, 1 987. This award is presented by the American Medical Association to physicians who have voluntarily
completed 1 50 hours of continuing medical education during a consecutive three-year time period. Of these 1 50
hours, at least 60 must be in AMA/PRA Category 1 . These seventeen individuals and the cities in which they reside
are presented below.

Baton Rouge

Francis A. Puyau, MD

Harvey

Sof Jan Lamid, MD*

Houma

Philip Royce Avet, MD

Jackson

Doyne Whittington Loyd, MD*

Lafayette

Donald Carl Harper, MD
Ricardo Roman Leoni, MD

Lake Charles

John Francis Raggio, MD

Monroe

Lowery Lee Thompson, MD

New Iberia

George Barry Cousin, MD

New Orleans

Luis Tomas Batista, MD*
Edward David Frohlich, MD
Deba Prasad Sarma, MD*

Shreveport

Horace Edwards Thompson, MD

Slidell

Kishore Vasudev Kamath, MD

Thibodaux

Neil James Maki, MD

Ville Platte

Adam John Tassin, Jr., MD

West Monroe

Gerald Melvin Robertson, MD

* These individuals are not members of the Louisiana State Medical Society

New this year . . .

One more reason to join the AM A

Special benefit packages available with 1988 membership

A diverse membership has diverse needs, and the AMA is committed to addressing
those needs. This year we’re introducing something new when you join the AMA or
renew your membership. In your AMA Membership Kit you’ll have the opportunity
to sign up for one of three benefit packages of publications, conferences, participa-
tory panels, focused issue updates, etc., on topics related to the area you designate.
Each package is tailored to address your particular interests:

■ Medical and scientific information and education designed to enhance your
practice, profession, and the public health.

■ Representation concentrated specifically on economic concerns, such as professional
liability and third party reimbursement.

■ Representation on a broad range of issues, including not only economic concerns,
but also quality of care, ethical issues, public health, and scientific issues.

To receive your full range of benefits, select one and only one of these free packages
by filling out the business reply card in your AMA Membership Kit.

Please look for the card in your AMA Membership Kit and return it promptly. Your
new benefit package is one more way the AMA supports you as a pnysician.

James H. Sammons, MD
Executive Vice President

HEALTH SCIENCn UIHAHT
UNIVERSITY OP MARYLAND
BALTIMORE

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TERRY R. JONES, MD
SHELDON P. KOITLE, MD
MAXIMO B. LAMARCHE, MD
PAUL B. LANSING, MD
SAMUEL A. LEONARD, MD
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JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY

1988

VOLUME 140 / NUMBER 4 /

APRIL

ARTICLES

Special issue: Cancer in Louisiana

Vivien W. Chen, PhD
Pelayo Correa, MD
Jean F. Craig, MS
Elizabeth T.H. Fontham, DPH

Is cancer survival poorer in
Louisiana?

Elizabeth T.H. Fontham, DPH
Pelayo Correa, MD
Vivien W. Chen, PhD
Jean F. Craig, MS
Linda W. Pickle, PhD
Roni Falk, MS

Tobacco and cancer

Pelayo Correa, MD
Elizabeth T.H. Fontham, DPH
Vivien W. Chen, PhD
Jean F. Craig, MS
Roni Falk, MS
Linda W. Pickle, PhD

Diet, nutrition, and cancer

Jean F. Craig, MS
Vivien W. Chen, PhD
Pelayo Correa, MD
Elizabeth T.H. Fontham, DPH

Louisiana Tumor Registry

Eleck Craig, MS
Charles L. Brown Jr, MD

Louisiana Cancer and
Lung Trust Fund Board

DEPARTMENTS

Information for Authors

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Calendar

ECG of the Month

Books Received

Otolaryngology/Head
& Neck Surgery Report

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Cover illustration by Eugene New, New Orleans.

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not omit digits.

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NEW MEMBERS

Applications for membership have been re-
ceived from the following physicians by the
respective parish medical societies as of Jan-
uary 13, 1988. The Louisiana State Medical
Society is pleased to welcome;

■ Calcasieu

Dewey D. Archer Jr, MD

2019 21st St, Lake Charles 70601

1983, Tulane University School of Medidne

psychiatry

Jake T. Hollen, MD

North Hwy 26, Box 1027, Jennings 70546
1976, University of Louisville School of
Medicine
internal medicine

Roger M. Williams, MD

2000 Oak Park Blvd, Lake Charles 70685
1982, LSU School of Medicine, Shreveport
otolaryngology

■ East Baton Rouge

Randall D. Lea, MD

1759 Physicians Park Dr, Baton Rouge 70816
1979> LSU School of Medicine, New Orleans
orthopedics

Jon V. Schellack, MD

5329 Didesse Dr, Baton Rouge 70808
1980, LSU School of Medidne, New Orleans
vascular surgery

Mark J. Waggenspack, MD

1113 S Range Ave, Suite B, Denham Springs
70727

1984, LSU School of Medicine, New Orleans
pediatrics

John G. Watts 111, MD

541 Shadows Lane, Suite A, Baton Rouge
70806

1984, Tulane University School of Medicine
pediatrics

■ Ouachita

LaDonna L. Ford, MD

4801 S Grand, Monroe 71201
1984, University of Arkansas School of
Medicine
internal medicine

Harvey T, Huddleston, MD

2601 River Oaks Dr, Monroe 71201
1962, University of Mississippi School of
Medidne

obstetrics & gynecology

Alfred D. Tisdale, MD

1400 Auburn, Monroe 71201

1958, Tulane University School of Medicine

pathology

■ Shreveport

Charles L. Black, MD

2510 Bert Koims Loop, Shreveport 71118

1980, LSU School of Medidne, Shreveport
general surgery

David A. Cavanaugh, MD

940 Margaret Place #210, Shreveport 71101

1981, LSU School of Medidne, Shreveport
neurosurgery

William H. Gallmaim 111, MD

PO Box 44123, Shreveport 71134

1980, Tulane University School of Medidne

diagnostic radiology

Terry W. Kendrick, MD

909 OHve St, Shreveport 71104

1984, LSU School of Medidne, Shreveport

pediatrics

■ St. Mary

Rand M. Dooley, MD

608 First, Morgan City 70380
1980, Facultad de Medidna de la Univer-
sidad de Guadalajara, Mexico
obstetrics & gynecology

■ Tri-Parish

Angela J. Gaskin, MD

402 E Green, Tallulah 71282

1982, Meharry Medical College, Nashville

family practice

■ Vermilion

Thomas D. Price, MD

710 North Foote, Kaplan 70548

1978, LSU School of Medicine, New Orleans

general practice

■ IntemI Resident Members

OUACHITA

Jose R. Enriquez, MD

1701 McKeen PI, Apt 68, Monroe 71201
1975, Faculty of Medidne and Surgery Uni-
versity of Santo Tomas, Philipptnes
family practice

JOURNAL VOL 140 APRIL 3

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Norton W. Voorhies, MD, Editor

ECG OF THE MONTH

I DON’T REMEMBER THE NAME

JORGE I. MARTINEZ-LOPEZ, MD

The six precordial leads shown below belong to a 64-year-old man and were recorded shortly after
admission to the hospital. No other information came with the tracing.

What is your diagnosis? Elucidation is on page 7.

JOURNAL VOL 140 APRIL 5

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helps build leaders.

FOR A FREE BROCHURE CALL THE DIRECTOR OF ADMISSI0NS-(601) 467-9057.

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ECG of the Month

Case presentation is on page 5.

DIAGNOSIS — Ventricular higeminy

The tracing is many years old, but it was pulled from
my files because it illustrates important points worthy
of emphasis; these will be the subject of the discussion
that follows.

DISCUSSION

First to draw the attention of the interpreter when
viewing the tracing is the repetitive pattern of cou-
plets, consisting of two QRS complexes of different
morphologies. This pattern can be termed ventricular
bigeminy and, because it is sustained, ventricular bi-
geminal rhythm. However, bigeminy is not an ECG di-
agnosis; instead, it is a descriptive term referring to
any of a number of disordered cardiac rhythms char-
acterized by paired impulses separated by pauses.
Bigeminal rhythms may arise from ectopic firing or
from failure of impulse formation or impulse con-
duction. Its presence, therefore, should evoke a search
for its many causes and an effort to define its precise
mechanism. Identification of the mechanism respon-
sible for bigeminal rhythm is crucial to management:
some require suppression, some require artificial car-
diac pacing, and others are innocuous.

Atrial activity is depicted by the presence of bi-
phasic (positive-negative) sinus P waves, best seen in
precordial lead VI. The P-P interval is regular, the
sinus rate is 65 a minute, and the P waves march
through both wide QRS complexes. This total lack of
temporal relationship between the Ps and the QRS
complexes is referred to as AV dissociation. But this
term, as is the case with bigeminy, is purely descrip-
tive and requires determination of its cause also.

It is proper now to analyze further the QRS com-
plexes; this will be done by using precordial lead VI
only. Both types of QRS complexes are abnormal in
appearance and exceed 0.12 sec in duration, but it has
to be determined whether they have a supraventric-
ular or a ventricular origin. The morphology of the
QRS complexes in VI is often useful in making this
determination. The odd-numbered QRS complexes
do not conform to the classic pattern recorded in pure
complete right bundle branch block; instead, they have

a monophasic configuration with a notch high on the
upstroke of the R wave and are consistent with ectopic
impulses originating in the left ventricle. By contrast,
the even-numbered QRS complexes in lead VI do
show the triphasic pattern typical of pure CRBBB.

This finding alone is a strong indication that the elec-
trical impulses responsible for the even-numbered QRS
complexes have a supraventricular origin and are con-
ducted downgrade with pure CRBBB. Thus, the first
QRS of the couplet is of left ventricular origin and the
second of supraventricular origin.

There are two other important findings in lead
VI. One is that a fixed coupling interval exists be-
tween the first and the second QRS of each couplet.

The other is that the interval between the second QRS
of a couplet and the first QRS of the next couplet is
longer, but also constant.

The interpreter should now examine lead V4. One
should detect the presence of small, negatively-ori-
ented spikes that recur regularly at 75 times a minute.
Closer inspection reveals that one spike occurs im-
mediately before the inscription of the first QRS of
the couplet, whereas the spike that follows it occurs
on the upstroke of the T wave of the second QRS of
the couplet. These spikes are consistent with the pres-
ence of an artificial cardiac pacemaker; the sequences
recorded indicate that the first QRS of each pair is a
"paced beat," whereas the second is not.

Having established the presence of an artificial
cardiac pacemaker, more information should be ex-
tracted from the tracing: the location of the pacing
electrode(s), whether the pacing electrode is unipolar
or bipolar, and the pacing mode of the pacemaker.

The first QRS of each pair is the paced QRS. Because
its morphology is consistent with left ventricular ec-
topy, it represents left ventricular epicardial pacing.

The small amplitude of the spikes resulting from pace-
maker firing suggests that the pacemaker electrode is
either bipolar or that two electrodes are present in
close proximity to each other on the left ventricular
surface. Finally, because the pacemaker fires con-
stantly and does not sense the second QRS of the
couplet, the inescapable conclusion is that it is a fixed-
rate (VOO) pacemaker.

The final solution to this tracing can now be sum-
marized. First, the basic cardiac rhythm is sinus at 65
times a minute. Second, AV dissociation is present ►

JOURNAL VOL 140 APRIL 7

and is the result of a functioning artificial cardiac pace-
maker. Third, the pacemaker is a fixed-rate mode, is
stimulating the left ventricular epicardium at 75 times
a minute, and is responsible for the first QRS of each
couplet. Finally, the second QRS of each couplet rep-
resents an AV junctional premature impulse — very
likely the result of reentry — that is conducted an-
terograde with CRBBB.

Left ventricular stimulation was performed many
years ago by inserting the pacing electrode directly
into the ventricular myocardium using open chest
surgery. The electrical system was bipolar and con-
sisted of two wires inserted in close proximity to each
other. The ECGs of patients in whom a left ventricular
epicardial pacemaker was implanted generally show
a RBBB pattern in the precordial leads and right axis
deviation in the frontal leads. Direct left ventricular
stimulation has been supplanted by pervenous right
ventricular endocardial stimulation.

At the beginning of this presentation, I men-
tioned that this was an old tracing. Upon recognizing

the pacemaker spikes, the reader may have thought:

'T don't remember the name (of the pacemaker) . . .

but the pace is familiar." ■

SELECTED REFERENCES

1. Rubin IL, Arbeit SR, Gross H: The electrocardiographic recognition of
pacemaker function and failiu-e. Ann Intern Med 1969;71:603-615.

2. Castellanos A Jr, Ortiz JM, Fastis N, et al: The electrocardiogram in pa-
tients with pacemakers. Prog Cardiovas Dis 1970;12:190-209.

3. Castellanos A, Lemberg L: Pacemaker arrhythmias and electrocardi-
ographic recognition of pacemakers. Circulation 1973;47:1382-1391.

4. Harthome JW: Indications for pacemaker insertion: Types and modes of
pacing. Prog Cardiovas Dis 1981;23:393-400.

Dr Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

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8 JOURNAL VOL 140 APRIL

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

IMMUNOTHERAPY OF
HEAD AND NECK CANCER:

AN OVERVIEW

ADRIAN WILLIAMSON III. MD: ROBERT H. MILLER. MD

Tumor immunotherapy has become a dynamic area
of research in the management of head and neck
cancer. With rapid developments in technology
and new understanding of tumor immunology, the
potential for immunological intervention in cancer
has increased. The purpose of this presentation is
to provide an introduction to immunotherapy of
head and neck cancer with a discussion of the

various modalities used.

T umor immunology has been an active field of can-
cer research for 100 years. The field of tumor im-
munotherapy was firmly established in 1943 by Lud-
wik Gross when he demonstrated that mice of a pure
inbred line could be immunized against a tumor that
originated in the same line.^ Until recently, most work
in immunotherapy of human cancer has been limited
to breast, ovarian, and colon-rectal cancer. With new
understanding of tumor immunology and improve-
ments in medical technology, the field has grown to
include all aspects of oncology, including head and
neck cancer.

Immunotherapy can be defined as ''the admin-
istration of any agent or treatment which stimulates,
modifies, or restores in a specific or nonspecific fash-
ion host immune reactivity and results in the regres-
sion or prophylaxis of tumors."^ Immunotherapy can
be categorized as active intervention, adoptive im-
munotherapy, passive immunotherapy, or immu-
nodepletive therapy (Table). ^

Active intervention may be achieved by vacci-
nation or by nonspecific augmentation of the immune
system with an immune stimulant. Although there
has been some success with inducing resistance to ►

JOURNAL VOL 140 APRIL 11

IMMUNOTHERAPY

Method

Agents Used

Active intervention

specific tumor vaccine
BCG

C. parvum
levamisole
thymic hormones
interferon
interleukin 2

Adoptive immunotherapy

leukocyte clones

Passive immunotherapy

monoclonal antibodies
antibody-toxin conjugates

Immunodepletive therapy

indomethacin

cimetidine

tumor challenge in animals, attempts to produce use-
ful vaccines for cancer of the head and neck have been
unsuccessful.^

Nonspecific immune system stimulants include
bacillus Calmette Guerin (BCG), Corynebacterium par-
vum, levamisole, thymic hormones, and lympho-
kines. BCG is employed as an attenuated strain of the
bacillus. It has been shown to be useful in animal
models with a small or limited tumor burden, and it
has been reported to prolong survival in acute mye-
logenous leukemia. However, BCG has not been of
significant benefit in head and neck cancer therapy.

Corynebacterium parvum contains no living or-
ganism and is made from phenol-killed bacteria. It
has been shown to prolong survival in breast cancer
and small cell cancer of the lung, but its use in head
and neck cancer has been disappointing.

Levamisole is an anthelminthic drug that appears
to enhance the immune reactivity in organisms whose
immunity is impaired. It has shown limited benefit
in patients with advanced breast and lung cancer but
it does not appear useful in head and neck cancer. ^
Like levamisole, thymic hormones enhance immunity
only when the immune reactivity is impaired. Thy-
mosin a 1 , has been shown to enhance in vitro pro-
duction of interleukin 2 (IL-2) in an animal model but
it has not been useful in clinical trials. ^

Currently, the most important lymphokines in
immunotherapy are interferon and IL-2. Interferon
has been most useful in the treatment of laryngeal
papilloma where up to 85% of treated patients have
shown improvement or stabilization of their disease.^

Recent studies of IL-2 have been promising. IL-2 has
been found to increase cytolytic T cell, macrophage,
and natural killer cell function in mice. Head and neck
cancer patients appear to be deficient in T cells that
produce IL-2.^

Adoptive immunotherapy is the transfer of tumor
immunity from one individual to another. Most work
in this aspect of immunotherapy is directed towards
cloning lymphocytes from a cancer patient's blood or
bone marrow. The lymphocytes could be stimulated
to develop antitumor properties against the patient's
tumor and then reinjected into the patient. This goal
has already been achieved in animal models.^

Passive immunotherapy involves administering
antitumor antibodies to patients in order to induce
tumor directed cytotoxic activity. Most work in this
field involves the use of monoclonal antibodies. These
antibodies are produced by the fusion of plasma ceU
tumors with normal lymphocytes that have been stim-
ulated against a tumor specific antigen. The resulting
tumor specific antibodies can be used in several ways.
Monoclonal antibodies have been shown to enhance
serologic cytotoxic factors (such as complement)
against human tumors. Currently there is much in-
terest in attaching cytotoxic agents to the antibody
and using the resulting "magic bullet" to cause non-
immunologic killing of the tumor cells. Finally, mon-
oclonal antibodies are being used in diagnosis of poorly
differentiated head and neck neoplasms and moni-
toring tumor recurrence.^

Immunodepletive therapy involves reducing
those factors that are immunosuppressive or inhibit
expression of tumor immunity. These factors include
prostaglandins, blocking antibodies, and suppressor
cell activity. Prostaglandins have been shown to cause
suppression of NK cell activity, decreased cell me-
diated tumoricidal function, and decreased produc-
tion of lymphokines. Up to 60% of squamous cell head
and neck cancer patients have increased levels of sup-
pressor monocytes that produce prostaglandin £ 2 -^
Some trials using indomethacin in head and neck can-
cer patients have been encouraging, although one
study using an animal model showed increased met-
astatic disease associated with indomethacin ther-
apy.^

An increase in the number of suppressor T cells
may result in the maintenance of certain tumors. It
has been shown that suppressor cell activity can be
blocked with cimetidine. Some trials have indicated

12 JOURNAL VOL 140 APRIL

that defects in cell mediated immunity in patients
with head and neck cancer can be reversed with ci-
metidine therapy.^

Other factors such as surgery, conventional
chemotherapy, radiation therapy, blood transfusions,
and poor nutrition can result in decreased immunity
in patients with head and neck cancer. All of these
considerations must be taken into account when eval-
uating immunity and immunotherapy in head and
neck cancer patients. ■

REFERENCES

1. Gross L: Intradermal immunization of C3H mice against a sarcoma that
originated in an animal of the same line. Cancer Res 1943;3(5):326-333.

I 2. Suen JY, Myers EN: Cancer of the Head and Neck. New York, Churchill
Livingstone, 1981.

3. Roitt I, Brostoff J, Male D: Immunology. London, Gower Medical Publish-
ing Ltd, 1985.

4. Cummings CW, Krause CJ: Otolaryngology — Head and Neck Surgery. St
Louis, CV Mosby Co, 1986, Vol 1.

5. McQuarrie DG: Head and Neck Cancer: Clinical Decisions and Management
Principles. Chicago, Year Book Medical Publishers Inc, 1986.

6. Wolf GT, Schmaltz S, Hudson J, et al: Alterations in T-lymphocyte sub-
populations in patients with head and neck cancer. Arch Otolaryngol Head
Neck Surg 1987;113(11):1200-1206.

7. Abemayor E, Kessler DJ, Ward PH, et al: Evaluation of poorly differen-
tiated head and neck neoplasms. Arch Otolaryngol Head Neck Surg
1987;113(5):506-509.

Dr. Williamson is a resident in the Dept of Otolaryngology-Head &
Neck Surgery at Tulane Medical School in New Orleans.

Dr. Miller is professor and chairman of the Dept of Otolaryngology-
Head & Neck Surgery at Tulane Medical School in New Orleans.

Reprints will not be available.

JOURNAL VOL 140 APRIL 13

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Jackie Tucker, LSMSA President

AUXILIARY REPORT

CONTINUITY IS THE KEY

SANCY McCOOL; JACKIE TUCKER

I MAGINE A BUSINESS that Operated on the principle
that each fiscal year was actually a “new" year, and
everything had to be evaluated in terms of starting at
the very begirming. Not only is it hard to imagine
someone trying to have a successful operation under
such circumstances, but it is equally hard to imagine
that the business could survive for very long. Just as
a house grows from a foundation, so a business, or
an organization, grows from what has gone before,
coupled with fresh and innovative ideas derived from
the new leaders each year.

We like to feel that our state Auxiliary has buQt
on the foundation laid and labored over by our parish
auxiliaries, and continues to grow and thrive with
input from our national leaders and state officers. Our
leadership seminars both within Louisiana and at
American Medical Association (AMA) Auxiliary head-
quarters in Chicago continue to inspire and encourage
our members with fresh ideas. Parish auxiliary visits
by our Louisiana State Medical Society Auxiliary pres-
ident and president-elect each year give members a
chance to talk with and discuss matters of importance,
and our annual state meeting gives each of us a chance
to evaluate our work for that year, and make plans
to improve the quality of the functions of that area in

the year to come.

Over the years, service needs have changed for
the Auxiliary. We still concentrate heavily on health
programs and projects for our communities, but we
now also stress legislation, aid to our medical schools
through AMA-Education and Research Foundation,
a support system for our members and their physician
spouses, and working with our state society in a team
concept of care and involvement.

With the demands becoming ever greater on the
medical community, it is imperative that we keep our
organization strong and viable. Increased member-
ship to fulfill our obligations is a "must," and each
physician spouse must be made aware of the necessity
of our organized efforts.

The foundation is strong, the leaders are dedi-
cated, the challenges are upon us. Now it is up to all
of us, as individual members, to make the dreams
reality. ■

Sancy McCool (wife of Dr E. Edward McCool) is the outgoing president
and Jackie Tucker (wife of Dr Robert Tucker) is the incoming president
of Louisiana State Medical Society Auxiliary.

JOURNAL VOL 140 APRIL 15

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June 20-23

1st International Symposium on Orbital Plastic Siu^ery, San

Francisco. Contact: Plastic Surgery Educational Foundation, 233
N Michigan Ave, Suite 1900, Chicago, IL 60601; (312)228-9900.

July

July 6-13

Breast Imaging and Ultrasound, Alaska 88: Cruise the In-
land Passage. Contact: Medical Seminars International Inc, 21915
Roscoe Blvd, Suite 222, Canoga Park, CA 91304; (818)719-7380.

July 14-16

4th Annual Berkshire Medical Conference: Advances in Car-
diology, Hancock, Massachusetts. Contact: Berkshire AHEC,
(413)447-2417.

July 17-22

Physicians and Their Families: Balancing Commitments to
Family and Profession, Estes Park, Colorado. Contact: Jayne
Roberts, Conference Coordinator, Division of Continuing Educa-
tion, The Menninger Clinic, Box 829, Topeka, KS 66601-0829;
(800)288-7377.

July 19-23

Louisiana Academy of Family Physicians Annual Scientific
Assembly, Sandestin Beach Hilton, Destin, Horida. (Contact:
LAPP, 4705 Iberville St, New Orleans, LA 70119.

July 24-28

34th Annual Southern OB-GYN Seminar, Asheville, North
Carolina. Contact: Dr. George Schneider, Ochsner Clinic, Dept
of OB-GYN, 1514 Jefferson Hwy, New Orleans, LA 70121;
(504)838-4031.

July 24-29

8th Aimual Internal Medicine Review, HQton Resort, South
Padre Island, Texas. Contact: Scott & White Continuing Medical
Education Office, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

July 21 - August 2
j Italy and the Swiss Alps, Sponsored by INTRAV and the
I Louisiana State Medical Society. Contact: Anita Bums, LSMS,

I 1700 Josephine St, New Orleans, LA 70113; (504)561-1033,

I (800)462-9508.

August

August 13-14

Anesthesia for the Cardiac Patient Having Non-Cardiac
Surgery, San Diego. Contact: American Society of Anesthe-
siologists, 515 Busse Hwy, Park Ridge, IL 60068.

August 21-30

INTRAV Cruise on the Queen Elizabeth 2 and London, Con-
tact: Anita Bums, Louisiana State Medical Society, 1700 Josephine
St, New Orleans, LA 70113; (504)561-1033, (800)462-9508.

September

September 10-18

4th Annual Fall Ultrasound Symposia, London and Paris.
Contact: Annual Fall Ultrasound Meeting, Medical Seminars In-
ternational Inc, 21915 Roscoe Blvd, Suite 222, Canoga Park, CA
91304; (818)719-7380.

September 14-19

Cosmetic Surgery of the Face and Breast, Monte Carlo,
Monaco. Contact: Francine Leinhardt, Conference Coordinator,
210 East 64th St, New York, NY 10021; (212)838-9200 ext 2776.

September 17-18

Metropolitan Regional Refresher Course, Las Vegas. Con-
tact: American Society of Anesthesiologists, 515 Busse Hwy, Park
Ridge, IL 60068.

October

October 3-7

6th Annual Comprehensive Review of Vascular Smgery,

Santa Monica, C^ornia. Contact: UCLA Extension, PO Box
24901, Los Angeles, CA 90024-0901; (213)825-1901.

October 8-12

American Society of Anesthesiologists Annual Meeting, San

Francisco. Contact: ASA, 515 Busse Hwy, Park Ridge, IL 60068.

JOURNAL VOL 140 APRIL 19

IS CANCER SURVIVAL POORER
IN LOUISIANA?

VIVIEN W. CHEN, PhD; PELAYO CORREA, MD,
JEAN F. CRAIG, MS; ELIZABETH T.H. FONTHAM, DPH

20 JOURNAL VOL 140 APRIL

Excess cancer mortality for selected sites has been
observed in Louisiana since the early 30s. At
present all four sex-race groups in Louisiana
experience higher mortality rates for all cancers
combined when compared to the national averages.
It is uncertain whether the higher death rates
result from higher incidence or poorer prognosis,
or a combination of both. To address the issue, we
examined data from the Louisiana Tumor Registry,
Charity Hospital Tumor Registry, and the
Surveillance, Epidemiology and End Results
program. Three measures were used for
comparison between the state and national data: (1)
incidence and mortality rates, (2) incidence/
mortality ratios, and (3) relative survival rates.
Poorer survival is observed for New Orleans and is
more evident among cancers with relatively better
prognosis. Possible reasons for this unfavorable
survival include socioeconomic factors, racial
factors, treatment variation, and host factors.

L ouisiana has been singled out as a community
displaying unusually high rates of cancer. Since
the early 30s, excess mortality rates for cancer of the
oral cavity and the respiratory system have been ob-
served. Between 1930 and 1932, the death rate for
cancer of buccal cavity and pharynx in Louisiana white
men was 50% higher than that of the United States
(9.7 per 100,000 vs 6.3) and double the rate (9.7 per
100,000 vs 4.9) for the southern region which included
the states of Alabama, Arkansas, Florida, Georgia,
Kentucky, Louisiana, Mississippi, North Carolina,
Oklahoma, South Carolina, Tennessee and Virginia.
Mortality for laryngeal cancer was 70% higher than
the national rate and more than triple the rate in the
south. Lung cancer, a rare cancer then, was also in
excess (4.0/100,000), 25% higher than the national av-
erage (3.2/100,000) and more than double the rate for
the south (1.7/100,000).! .

Death rates for cancers of the respiratory tract,
in particular lung cancer, have risen sharply since
1930, both in Louisiana and nationwide and, since the
mid-50s, have become the leading cause of cancer
death in men. The lung cancer death rate in Louisiana
white men has increased tenfold from the 30s (4.0/
100,000) to the 50s (41.3/100,000) and doubled from
the 50s to 70s (80/100,000) to become the nation's high-
est lung cancer death rate. The rate of increase in the

United States was similar for the corresponding pe-
riods, from 3.2/100,000 to 29.6 to 64.0.^

Since lung cancer became the leading cause of
cancer death in men nationwide, and since Louisiana
showed the highest lung cancer rate, the mortality
rate for all cancers combined in Louisiana white males
also exceeded the national rate in the 50s. In addition,
cancer mortality of all sites for black males surpassed
that of white males in 1964 to become the highest
among the four sex-race groups. To date, mortality
rates for all cancers combined in Louisiana remain
higher than the national averages for all four groups.

Despite the consistent observations of higher
rates, a question remains unanswered. Are the ex-
cessive cancer death rates experienced by Louisiana
residents a result of a higher risk (ie, higher incidence
rates), a poorer prognosis, or a combination of both?
In order to address the issue, we examine data from
the Louisiana Tumor Registry (LTR), the Tumor Reg-
istry of Charity Hospital at New Orleans, the End
Results Program of National Cancer Institute (NCI),
the Surveillance, Epidemiology and End Results
(SEER) program of the NCI and the National Center
for Health Statistics. Three different measures are used
for the following comparisons between national and
state data: (1) incidence and mortality rates, (2) inci-
dence/mortality ratios, and (3) relative survival rates.

INCIDENCE AND MORTALITY RATES

Incidence rates are the best estimates of cancer risk
in a population. The LTR has been collecting inci-
dence data for metropolitan New Orleans (Jefferson,
Orleans, and St Bernard parishes) since 1974. The
registry expanded to the whole southern region in
1983, to the northeast region in 1985, and to the Al-
exandria and Shreveport areas in 1987. Since it takes
several years to accumulate data for incidence cal-
culation, such data are currently available for the New
Orleans area only. Therefore, cancer incidence for New
Orleans only is compared to the national averages,
obtained from the combined experience of the group
of population-based registries which constitute the
SEER program. The participants include five entire
states and five metropolitan areas: Connecticut, Iowa,
New Mexico, Utah, Hawaii, Detroit, Atlanta, New
Orleans, Seattle-Puget Sound and San Francisco-Oak-
land.^

JOURNAL VOL 140 APRIL 21

TABLE 1

AVERAGE ANNUAL AGE-ADJUSTED (US 1970 STANDARD) INCIDENCE AND MORTALITY RATE PER 100,000 POPULATION
AND INCIDENCE/MORTALITY RATIO BY PRIMARY SITE, RACE AND SEX IN NEW ORLEANS AND ALL SEER AREAS

(EXCLUDING PUERTO RICO), 1973-1977

New Orleans

All SEER Areas

Incidence

Mortality

I/M

Incidence

Mortality

I/M

All sites

412.4

258.7

1.59

371.6

209.5

1.77

270.8

141.5

1.91

301.2

136.9

2.20

480.8

329.3

1.46

454.3

292.1

1.56

282.3

181.8

1.55

288.7

160.6

1.80

Oral Cavity

22.3

11.3

1.97

16.8

5.8

2.90

& Pharynx

6.6

1.6

4.13

6.0

2.0

3.00

26.8

13.4

2.00

19.3

9.0

2.14

8.2

3.3

2.48

7.0

2.5

2.80

Esophagus

4.6

5.8

0.79

4.8

4.9

1.00

0.7

1.0

0.70

1.6

1.5

1.07

16.6

12.4

1.34

16.9

15.0

1.13

3.6

2.7

1.33

4.5

3.9

1.15

Stomach

9.8

6.9

1.42

12.7

9.5

1.34

4.8

4.5

1.07

5.6

4.5

1.24

29.0

21.4

1.36

22.4

17.1

1.31

13.3

10.9

1.22

9.9

7.4

1.34

Colon

37.1

25.4

1.46

36.7

21.3

1.72

27.3

15.9

1.72

31.0

16.9

1.83

31.5

18.3

1.72

36.3

20.9

1.74

30.9

16.4

1.88

30.6

17.4

1.76

Rectum

20.4

7.6

2.68

19.1

5.7

3.35

9.6

3.3

2.91

11.5

3.3

3.48

17.0

9.6

1.77

13.3

6.3

2.11

9.3

5.0

1.86

10.5

3.6

2.92

Pancreas

12.9

11.7

1.10

11.9

11.4

1.04

9.6

8.5

1.13

7.7

7.3

1.05

18.7

14.4

1.30

17.5

15.7

1.11

8.9

7.8

1.14

11.9

10.2

1.17

Larynx

10.7

3.6

2.97

8.3

2.7

3.07

1.7

0.4

4.25

1.3

0.4

3.25

14.7

3.3

4.45

12.1

4.5

2.69

2.1

0.5

4.20

1.9

0.6

3.17

As shown in Table 1, New Orleanians, when
compared to those residing in the SEER areas, display
excessive rates for certain cancers not only in mortality
but also in incidence, the latter indicating a higher
risk of acquiring the disease. The excessive rates in-
clude; lung cancer for all four sex-race groups, cancer
of the oral cavity and pharynx for all except white
females, cancer of all sites and rectum for males only,
stomach cancer for blacks of both sexes, and cancers
of the pancreas, larynx, bladder, and kidney for whites
of both sexes. Therefore, the observed higher mor-
tality rates are at least in part the result of a higher
risk of acquiring the disease.

Excessive mortality from all cancers combined is
observed for white females in New Orleans when
compared to the SEER average even though they ex-
perience a lower incidence rate. Similarly, lower in-
cidence contrasting with higher mortality is observed
for breast cancer among New Orleans women (both
black and white) and for cancers of the urinary tract
in black males. These findings suggest poorer survival
for New Orleans patients with such cancers.

INCIDENCE/MORTALITY RATIOS

The ratio of incidence rate to mortality rate (I/M) is a

22 JOURNAL VOL 140 APRIL

TABLE 1 (continued)

New Orleans

All SEER Areas

Incidence

Mortality

I/M

Incidence

Mortality

I/M

Lung

107.6

84.8

1.27

76.4

62.5

1.22

27.4

19.6

1.40

21.8

16.2

1.35

129.6

105.2

1.23

110.0

92.6

1.19

27.5

18.4

1.49

24.3

17.6

1.38

Breast

78.1

28.7

2.72

85.6

28.4

3.01

67.5

30.3

2.23

72.0

27.8

2.59

Cervix

9.8

2.9

3.38

10.9

3.5

3.11

(invasive)

24.4

9.9

2.46

25.7

10.5

2.45

Corpus

12.5

1.3

9.62

29.9

1.9

15.74

13.3

3.1

4.29

14.6

3.1

4.71

Prostate

55.7

21.2

2.63

66.2

22.0

3.01

100.8

39.3

2.56

108.9

41.1

2.65

Bladder

32.9

9.2

3.58

27.0

7.7

3.51

8.6

3.1

2.77

7.1

2.2

3.23

11.8

5.4

2.19

13.6

5.3

2.57

5.1

2.2

2.32

5.5

3.4

1.62

Kidney

10.9

6.0

1.82

9.4

4.4

2.14

4.8

2.5

1.92

4.4

2.0

2.20

7.5

4.9

1.53

8.7

4.2

2.07

3.2

0.8

4.00

4.4

1.8

2.44

Brain &

7.6

5.1

1.49

6.7

5.1

1.31

CNS

4.6

3.2

1.44

4.6

3.3

1.39

4.3

4.5

0.96

4.2

3.4

1.24

3.7

1.9

1.95

2.7

1.9

1.42

Lymphoma

14.2

8.2

1.73

14.3

7.7

1.86

10.4

5.5

1.89

10.7

5.2

2.06

8.4

4.9

1.71

10.3

5.6

1.84

5.1

3.2

1.59

5.8

3.2

1.81

Leukemia

11.6

9.9

1.17

13.0

9.3

1.40

6.4

5.2

1.23

7.7

5.2

1.48

9.1

8.9

1.02

11.1

8.0

1.39

6.6

7.0

0.94

6.8

4.7

1.45

crude measure of prognosis. If the I/M ratio approx-
imates one, with mortality approaching incidence, it
reflects extremely poor prognosis. On the other hand,
a high I/M ratio indicates good prognosis.

As shown in Table 1, I/M ratios for many cancer
sites are lower in New Orleans than in the SEER areas.
The poorer survival is more evident among cancers
which in general have good prognosis (ie, cancer of
the rectum, female breast, uterine corpus, prostate,
and kidney). For cancers with very poor prognosis
such as lung, pancreas and stomach, similar ratios are

observed between New Orleans and SEER areas.

In addition, lower I/M ratios are observed among
New Orleans blacks when compared to New Orleans
whites, a phenomenon which is consistent with the
national findings, ie, a poorer survival among black
cancer patients.^' ^

Since the I/M ratio does not take the staging of
disease into account, the observed poorer survival in
New Orleans could be partially explained by a larger
proportion of patients with advanced disease at the
time of diagnosis.

JOURNAL VOL 140 APRIL 23

BECAUSE

ONIY

ISAIWAYS

REMEMBER TO WRITE “DO NOT SUBSTITUTE.”
IT PROTECTS YOUR DECISION.

The cut out "V" design is a registered trademark of Roche Products Inc.

Charity Hospital

1 948- 1 984 National Rates

1950-1954* 1965-1969* 1977-1 981 1

Esophagus

—

Stomach

Colon

Rectum

Pancreas

—

Larynx

—

Lung

Breast

Cervix

Corpus

Prostate

Kidney

—

Bladder

Brain

—

RELATIVE SURVIVAL RATE

The relative survival rate is generally considered the
best estimate of prognosis for cancer patients. It is the
ratio of the observed survival rate to the expected
survival rate for persons from the general population
who are similar to the patient group with respect to
age, race, sex and calendar period of observation. The
relative survival rate can be interpreted as an estimate
of the probability of escaping causes of death related
to the diagnosed cancer. It can also be calculated for
specific race, sex, and stage of disease at diagnosis.

In order to compute survival rates, active follow-
up of each patient under study is necessary. Unfor-
tunately, this type of active follow-up is extremely
time-consuming and very expensive, and is, there-
fore, usually performed in hospital settings only. The
LTR routinely collects only passive survival infor-
mation based on linking mortality computer tapes with
the master incidence file. Charity Hospital at New
Orleans, one of the nation's oldest and the state's first
tumor registry, collects active follow-up data. It began

its operation in 1947 and has data available since 1948.
Therefore, it is selected for comparison with the na-
tional data.

Table 2 presents five-year relative survival rates
for cancer patients in Charity Hospital with localized
disease only and compared to the corresponding na-
tional figures.^ The national survival rates for the two
earlier periods, 1950-1954 and 1965-1969^ are from the
previous End Results Program of NCI (which has
evolved and expanded to the present SEER program)
while data for the latest period come from SEER reg-
istries.^ Even though we are comparing cancer pa-
tients with the same stage of disease (localized dis-
ease) and by race (black and white separately), a poorer
survival is observed for Charity Hospital patients when
compared to those of the End Results Program of the
NCI and the SEER program. As noted previously, the
difference is more marked for cancers of the rectum,
female breast, and uterine corpus.

It should be noted that the survival data from
Charity Hospital cover a very wide range of time,
during which major breakthroughs in treatment and ►

JOURNAL VOL 140 APRIL 25

improvement in survival have occurred. However,
due to the lack of computer support at the Charity
Hospital Tumor Registry at present, comparisons us-
ing same time-periods are not possible. Even so, when
compared to the national rates for the period 1950-
1954, survival deficits are observed for Charity white
patients. Since Charity patients are not representative
of cancer patients in Louisiana at large, survival data
from a more comparable private hospital was ex-
plored. Touro Hospital has had a tumor registry in
operation since 1958. Unfortunately, cases diagnosed
prior to 1982 are not entered in a computer, and the
available data consist of manually computed crude
survival rates which cannot be compared with the
relative survival rates.

DISCUSSION

To explore the reasons for the poor survival in Lou-
isiana the following factors should be taken into ac-
count:

1 . Socioeconomic factors .

Numerous earlier studies have suggested socioeco-
nomic factors to be the main determinant of survival
difference among cancer patients. "Low-income" pa-
tients do not do as well as the "affluent" private pa-
tients. Poorer survival rates have been found in three
studies comparing: low-income with high-income pa-
tients; non-private or indigent hospital patients with
private patients; and public hospital patients with pri-
vate hospital patients. The survival deficit remains
even after adjusting for stage of the disease, treat-
ment, and quality of care.^^ The data shown in Table
2 reflect in a major way socioeconomic factors because
low income Charity Hospital patients are compared
with national figures in which higher income patients
predominate.

2. Racial factors.

A black/white survival differential in cancer patients
has been observed since the 50s. The large survival
disadvantage for black patients is in part due to a
higher proportion of advanced or non-localized dis-
ease at the time of diagnosis, confounded further by
socioeconomic factors. Adjusting for age and stage of
disease narrows the gap of overall survival rates but
falls far short of explaining the significant black/white
difference.®' In a 10-year follow-up study on breast
cancer patients treated at M.D. Anderson Hospital,

Westbrook et al found that blacks and Chicanos with
"early" diseases had a significantly worse survival
rate than whites with the same stage of disease.

3. Treatment variation.

The poorer survival among public hospital patients is
generally ascribed to lower socioeconomic status. Since
indigent and non-indigent patients are usually treated
in different hospitals and by different medical staffs,
treatment and quality of care variation cannot be ex-
cluded as a prognostic factor. In California county
hospitals, attended mostly by non-whites and lower
socioeconomic patients, less surgery for colon cancer
patients was performed than in private hospitals.^®
Page and Kuntz^® studied the survival experience of
46,000 Veteran Administration (VA) male cancer pa-
tients and found no significant differences between
black and white patients except for bladder cancer.
They suggested that their findings, which differed
from those in other studies, were due to the fact that
all veteran patients receive the same treatment with-
out regard to socioeconomic class or ability to pay.
They further concluded that, when treatment and
quality of care were the same, socioeconomic factors
and race do not generally affect survival experience.
However, the patient population seeking care at VA
hospitals does not provide the same contrast existing
between private and Charity Hospitals clientele.

4. Host factor.

Host differences associated with poverty have been
postulated by Berg et al to account for much of the
observed difference in survival rates, whether it is
between black and white, indigent and non-indigent,
or public and private patients. He studied the rela-
tionship between economic status and survival for
numerous types of cancer among patients of the Uni-
versity of Iowa Hospital and found a substantial sur-
vival difference between indigent patients and clinic-
pay patients. These two groups of teaching patients,
almost all of them white, received the same quality
of care, but the clinic-pay patients were of higher
economic status. Differences in age at diagnosis and
stage of disease were estimated to account for less
than half of the survival deficit in the indigents; the
rest of the deficit was associated with the low eco-
nomic status.

The association between indigency and poor sur-
vival may be a reflection of host vulnerability. Poor
general health may influence the choice of treatment

26 JOURNAL VOL 140 APRIL

which can in turn affect survival. Low income may
also result in poor nutrition and poor biological im-
munocompetence .

All of the aforementioned factors are interrelated
and are possible reasons for the apparent poorer sur-
vival in Louisiana. Approximately 30% of the popu-
lation in Louisiana is black and a larger proportion of
our residents have income below the poverty level:
18.6% vs 14.0% nationally. In the Ten State Nu-
trition Survey, low intake of vitamin A was found in
southern parishes where cancer rates were high and
serum vitarnin C was deficient in 15% of the low-
income residents. Research on the effect of nutrition
on cancer incidence and survival in Louisiana is much
needed.

Since 1985, we have been conducting a study to
investigate the black/white prognosis difference in
New Orleans patients with cancer of the breast, colon,
uterine corpus, or urinary bladder. The study is con-
ducted in collaboration with the NCI and researchers
in Atlanta and San Francisco. The study attempts to
explore the racial differences in nutrition, smoking
and alcohol consumption, social support from family
and friends, symptom recognition, delay in seeking
care and entering the health care system, financial
resources, and compliance with treatment as weU as
morphologic characteristics of the primary tumor.

Preliminary analyses of the study show that a
smaller proportion of black patients recognize cancer-
related symptoms, as compared to the whites. They
also delay longer before seeking care and, when they
do, it is more often for reasons other than tumor-
related symptoms. Furthermore, there is some indi-
cation of nutritrional deficiency among the black pa-
tients. We hope that upon completion of the study,
we will have a better understanding of the reasons
for survival differential, not only between black and
white patients, but between Louisiana and other areas
in the nation.

In conclusion, it would appear that in Louisiana
the high incidence of cancer and the poorer survival
of cancer patients is mostly related to factors linked
with low socioeconomic status and the existence of a
large indigent population. ■

ACKNOWLEDGMENT

We would like to take the opportunity to thank the
following 24 hospitals, their adrrdnistrators and med-

ical staff, for participating in this BlackAVhite Prog-
nosis Study. These include all hospitals treating can-
cer patients in greater New Orleans except one. They
are: Chalmette General Hospital, Charity Hospital at
New Orleans, De La Ronde Hospital, Doctor's Hos-
pital, East Jefferson General Hospital, ELmwood Med-
ical Center (formerly Bonnabel Hospital), Flint-Good-
ridge Hospital (1985 only). Hotel Dieu Hospital,
Humana Woman's Hospital, Lakeside Hospital, Mea-
dowcrest Hospital, Mercy Hospital, Montelepre Me-
morial Hospital, New Orleans General Hospital,
Ochsner Foundation Hospital and Clinics, Pendleton
Memorial Methodist Hospital, Jo Ellen Smith Me-
morial Hospital, Southern Baptist Hospital, St Jude
Hospital, Touro Infirmary, Tulane Medical Center,
United Medical Center, Veteran Administration Hos-
pital at New Orleans, and West Jefferson General
Hospital. In addition, we are grateful for the partic-
ipation of private radiation centers and private pa-
thology laboratories. We also would Hke to extend
our appreciation to aU clinicians, especially surgeons
and oncologists, whose cooperation and support are
essential for this study. Special thanks go to the staff
of the medical records department and pathology de-
partment of each hospital; without their assistance,
the study would have been an impossible task for our
research team.

This work was supported by Grant #N01-CP-
43262 and Contract #N01-CN-45175.

REFERENCES

1. Cover M: Cancer Mortality in the United States, III. Geographic Variation in
Recorded Cancer Mortality for Detailed Sites, for an Average of the Years 1930-
32, Public Health Bulletin No. 257. US Public Health Service, 1940.

2. Riggan WB, Van Bruggen J, Mason T, et al: US Cancer Mortality Rates
and Trends, 1950-79, vol 1. National Cancer Institute/Environmental Pro-
tection Agency, 1983.

3. Young JL, Percy CL, Asire AJ: Surveillance, Epidemiology and End Results:
Incidence and Mortality Data, 1973-77, Dept of Health and Human Services
publication No. (NIH) 81-2330. National Cancer Institute, 1981.

4. AxteU LM, Myers MH: Contrasts in survival of black and white cancer
patients, 1960-73. JNCI 1978;60:1209-1215.

5. Sondik E, Yormg JL, Horm JW, et al: National Cancer Advisory Board:
Annual Cancer Statistics Review. Dept of Health and Hmnan Services 1984.

6. Carter RD, Faddis D, Krementz E, et al: Charity Hospital Tumor Registry,
1948-84. New Orleans, Charity Hospital of Louisiana, 1986.

7. AxteU LM, Asire AJ, Myers MH: Cancer Patient Survival Report No. 5,
Dept of Health, Educational Welfare publication No. (NIH) 77-992, 1976.

8. Cancer Registration and Survival in California. Berkeley, State of CaUfomia
Dept of Public Health, California Tumor Registry; 1963.

9. Lipworth L, AbeUn T, CormeUy RR: Socioeconomic factors in the prog-
nosis of cancer patients. } Chronic Dis 1970;23:105-115.

10. Lipworth L, Bennett R, Parker P: Prognosis of nonprivate cancer pa-
tients. JNCI 1972;48:11-16.

JOURNAL VOL 140 APRIL 27

11. Berg JW, Ross R, Latourette HB: Economic status and survival of cancer
patients. Cancer 1977;39A67-477 .

12. Myer MH, Hankey BE: Comparison of survival for black and white pa-
tients, in Cancer Patient Survival Experience. Dept of Health and Human
Services PubUcation No. (NIH) 80-2148, 1980.

13. Myer MH: Survival from cancer by blacks and whites, in Cancer Among
Black Populations, Mettlin C, Murphy GP (eds). New York, Alan R Liss
Inc 1981.

14. Westbrook KC, Brown BW, McBride CM: Breast cancer: A critical review
of a patient sample with a ten-year follow-up. South Med J 1975;68:543-
548.

15. Krain LS: Racial and socioeconomic factors in colon cancer mortality.
Oncology 1972;26:335-344.

16. Page WF, Kuntz AZ: Racial and socioeconomic factors in cancer survival.
Cancer 1980;45:1029-1040.

17. 1980 Census of Population: General Social and Economic Characteristics —
Louisiana, PC80-1-C20. US Dept of Commerce, Bureau of the Census,
1983.

18. Health Status of Minorities and Low Income Groups. Dept of Health and
Human Resources publication No. (HRSA) HRS-P-DV 85-1. Health Re-
sources and Services Administration, 1985.

19. Ten-state nutrition survey, 1968-70, US Dept Health, Education and Wel-
fare 72-8129, 72-8130, 72-8131, 72-8132, 72-8133, 1972.

Drs Chen, Correa, and Fontham are from the Dept of Pathology at LSU
Medical Center in New Orleans. Dr Chen is also affiliated with the
Dept of Biostatistics and Epidemiology at Tulane University School of
Public Health and Tropical Medicine in New Orleans.

Ms Craig is from the Louisiana Tumor Registry in the Dept of Health
and Human Resources in New Orleans.

Reprint requests should be sent to Vivien W. Chen, PhD, Dept of
Pathology, LSU Medical Center, 1901 Perdido St,
New Orleans, LA 70112.

28 JOURNAL VOL 140 APRIL

YOCON'

YOHIMBINE HCI

Description; Yohimbine is a 3a-15a-20B-17a-hydroxy Yohimbine-16a-car-
boxylic acid methyl ester. The alkaloid is found in Rubaceae and related trees.
Also in Rauwolfia Serpentina (L) Benth. Yohimbine is an indolalkylamine
alkaloid with chemical similarity to reserpine. it is a crystalline powder,
odorless. Each compressed tablet contains (1/12 gr.) 5.4 mg of Yohimbine
Hydrochloride.

Action: Yohimbine blocks presynaptic alpha-2 adrenergic receptors. Its
action on peripheral blood vessels resembles that of reserpine, though it is
weaker and of short duration. Yohimbine’s peripheral autonomic nervous
system effect is to increase parasympathetic (cholinergic) and decrease
sympattietic (adrenergic) activity. It is to be noted that in male sexual
performance, erection is linked to cholinergic activity and to alpha-2 ad-
renergic blockade which may theoretically result in increased penile inflow,
decreased penile outflow or both.

Reportedly, Yohimbine exerts no significant influence on cardiac stimula-
tion and other effects mediated by B-adrenergic receptors, its effect on blood
pressure, if any, would be to lower it; however no adequate studies are at hand
to quantitate this effect in terms of Yohimbine dosage,
indications; Yocon® is indicated as a sympathicolytic and mydriatric. It may
have activity as an aphrodisiac.

Contraindications: Renal diseases, and patient’s sensitive to the drug. In
view of the limited and inadequate information at hand, no precise tabulation
can be offered of additional contraindications.

Warning: Generally, this drug is not proposed for use in females and certainly
must not be used during pregnancy. Neither is this drug proposed for use in
pediatric, geriatric or cardio-renal patients with gastric or duodenal ulcer
history. Nor should it be used in conjunction with mood-modifying drugs
such as antidepressants, or in psychiatric patients in general.

Adverse Reactions: Yohimbine readily penetrates the (CNS) and produces a
complex pattern of responses in lower doses than required to produce periph-
eral a-adrenergic blockade. These include, anti-diuresis, a general picture of
central excitation including elevation of blood pressure and heart rate, in-
creased motor activity, irritability and tremor. Sweating, nausea and vomiting
are common after parenteral administration of the drug.T2 Also dizziness,
headache, skin flushing reported when used orally.T3
Dosage and Administration: Experimental dosage reported in treatment of
erectile impotence. ^ ^ 1 tablet (5.4 mg) 3 times a day, to adult males taken
orally. Occasional side effects reported with this dosage are nausea, dizziness
or nervousness. In the event of side effects dosage to be reduced to Vi tablet 3
times a day, followed by gradual increases to 1 tablet 3 times a day. Reported
therapy not more than 10 weeks.3
How Supplied: Oral tablets of Yocon® 1/12 gr. 5.4 mg in

bottles of 100’s NDC 53159-001-01 and 1000’s NDC

53159-001-10.

References;

1. A. Morales et al.. New England Journal of Medi-
cine; 1221 . November 12, 1981 .

2. Goodman, Gilman — The Pharmacological basis
of Therapeutics 6th ed . , p . 1 76 - 1 88.

McMillan December Rev. 1/85.

3. Weekly Urological Clinical letter, 27:2, July 4,

1983.

4. A. Morales et al. , The Journal of Urology 128:

45-47, 1982.

Rev. 1/85

AVAILABLE EXCLUSIVELY FROM

PALISADES

PHARMACEUTICALS, INC.

219 County Road
Tenafly, New Jersey 07670

(201) 569-8502
Outside NJ 1-800-237-9083

TOBACCO AND CANCER

ELIZABETH T.H. FONTHAM, DPH; PELAYO CORREA, MD;
VIVIEN W. CHEN, PhD; JEAN F. CRAIG, MS;

LINDA W. PICKLE, PhD; RONI FALK, MS

Much of the excess cancer risk in Louisiana derives
from those cancers strongly associated with tobacco
use. The Cancer Epidemiology Research Unit of
LSU Medical Center Department of Pathology has
conducted a series of studies in Louisiana which
examined the etiology of cancers of the lung,
stomach, pancreas, oral cavity, cervix, and bladder.
Findings indicate that approximately 90% of the
lung cancer is attributable to active cigarette
smoking. Passive smoke exposure was found to
increase risk of lung cancer one and one-half to
three-fold among non-smokers married to smokers.
Smoking of cigars and pipes had a more consistent
association with risk of stomach cancer than did
cigarette smoking. A significant increasing risk of
pancreatic cancer with increasing number of
cigarettes smoked was seen. Evidence of tobacco-
induced chromosome damage was found in
epithelial cells from the oral cavity, urinary
bladder, and uterine cervix consistent with
increased risk of these cancers among smokers.

A ny consideration of chronic disease in general,
and cancer in particular, which does not include
the role of tobacco ignores the single most important
causal factor. Recent risk estimates indicate that to-
bacco's contribution to all cancer deaths is approxi-
mately 30%.^ The only other factor which may have
an impact of this magnitude on cancer causation is
diet. Unlike tobacco, dietary factors may exert a pos-
itive or negative effect on cancer risk and will be dis-
cussed separately in this issue.

What are the tobacco-related cancers and how do
Louisiana rates compare with the rest of the country?
The tobacco-related cancers are listed in Table 1 with
comparative incidence and mortality rates for the race-
sex group in which that cancer is of particular im-
portance. The rates for each cancer for all sex-race
groups appear in the preceding article {Is cancer sur-
vival poorer in Louisiana? by Chen et al). For some sites
the association between tobacco use and cancer is
weU-documented and clearly causal; for others, the
association is less well understood. Almost without
exception, Louisiana tobacco-related cancer rates are
higher than the rates for the other areas of the United
States. The most striking disparity is for lung cancer,
which alone accounts for one-fourth of all cancer

JOURNAL VOL 140 APRIL 29

TABLE 1

TOBACCO-RELATED CANCERS; MORTALITY AND INCIDENCE

1970-1979 Average Annual Age

1978-1981 Average Annual Age

Adjusted Mortality Rates Per 100,000

Adjusted Incidence Rates Per 100,000

National

Metropolitan

Site

Louisiana

Average

N.O.

SEER*

Lung (WM)

80.0

64.0

104.7

81.0

Larynx (WM)

2.9

2.7

12.9

8.4

Oral Cavity (WM)

6.4

5.2

20.5

16.8

Esophagus (BM)

10.8

12.3

18.6

Bladder (WM)

6.9

7.3

28.6

27.3

Pancreas (WM)

12.9

10.9

12.5

10.9

Stomach (BM)

19.4

16.2

22.4

21.3

Cervix (BF)

11.6

10.2

20.0

20.2

* SEER: Surveillance Epidemiology End Results, a continuing project of the National Cancer Institute which funds population-based tumor
registries at various sites throughout the United States,
t Not available

deaths in this country. Incidence and mortality rates
in Louisiana are 25% higher than in other areas of the
country. Lung cancer incidence rates in New Orleans
for black males are the highest on record internation-
ally: 107/100,000 per year (adjusted to the "'world"
population); or 13.6 cumulative rate ages 0-74, roughly
indicating that approximately 13.6% of black males in
New Orleans wUl develop lung cancer. ^

Since the late 70s, a number of epidemiologic
studies which focused on the etiology of these cancers
have been conducted in Louisiana. The main findings
of these studies as related to tobacco will be briefly
discussed.

ACTIVE SMOKING

Lung Cancer

A survey of adult males in south and north Louisiana
was conducted to explore lifestyle and environmental
factors which might explain the high cancer rates in
the southern part of the state compared to the north-
ern part.^ The proportion of current smokers and the
level of non-filter cigarette use were both higher in
south Louisiana. Smokers in the southern region re-
ported starting at an earlier age than their northern
counterparts. In addition, a larger proportion of whites
living in the south reported that their parents had

30 JOURNAL VOL 140 APRIL

smoked, which indicates that the current excess of
smokers extends back at least one generation. These
findings suggested that at least one factor in the high
lung cancer rates seen in south Louisiana was likely
the amount and manner of cigarette smoking in that
region.

A case-control study of lung cancer was then in-
itiated in a 26-parish area covering south Louisiana.
Current primary lung cancer cases were identified
from hospital admission and pathology records in
hospitals. All the major hospitals in the study area
participated except in the New Orleans metropolitan
area where, by design, a sample was taken of the
public and private hospitals accounting for approxi-
mately half the lung cancer cases in the city. A control
was randomly selected from patients attending the
same hospital matched by race, sex, and age (within
five years). Interviews were completed for 1,253 cases
and 1,274 controls, representing 76% and 85% of those
eligible respectively. An extensive questionnaire ob-
tained information concerning tobacco use, diet, oc-
cupational, residential, medical, and family histories.

As noted in the first published report of this study,
"in terms of the magnitude of risks and the proportion
of the population exposed to the risk factors, cigarette
smoking overshadows all other factors."^ There were
few cases who had never smoked: 97.7% of white

TABLE 2

ESTIMATED RELATIVE RISK OF LUNG CANCER ACCORDING TO HISTORY OF CIGARETTE USE BY HISTOLOGIC TYPE

Number of
Cases

All Lung
Cancers

Squamous and
Small Cell
Carcinomas

Adenocarcinomas

Never smoked

1.0

Ever smoked

1201

11.4

28.3

5.6

Ex-smoker

258

6.5

15.5

3.7

Current smoker

943

14.2

34.6

6.7

1 -20 cig/day

371

9.3

23.2

4.3

21 - 1 - cig/day

514

25.3

54.8

12.0

male lung cancer cases, 97.6% of black males, 88% of
white females, and 94% of black female cases had
smoked. Table 2 presents the risk of all types of lung
carcinoma associated with cigarette use as well as a
separate consideration of risk by histologic type. For
heavy current smokers in Louisiana the risk of lung
cancer is 25 times that of a non-smoker. While risk of
squamous and small cell carcinomas (Kreyberg I) is
clearly the most striking, a 12-fold increased risk of
adenocarcinoma among persons smoking more than
one pack a day is many times higher than any other
known risk factor for adenocarcinoma of the lung.

Estimates of relative risk of lung cancer shown
in Table 3 indicate increasing risk of lung cancer for
non-filter only versus filter only relative to non-smok-
ers. The adverse effects of depth of inhalation, early
initiation of cigarette smoking, and failure to stop
smoking are also quantified. While other risk factors
for lung cancer have been delineated by this study,
estimates of attributable risk indicate that as much as
90% of lung cancer in this region is attributable to
cigarette smoking.

Stomach Cancer

All investigations to date of gastric cancer have im-
plicated diet as the major determinant of gastric can-
cer risk. Smoking has been examined as a risk factor
for this disease, but the findings have been equivocal.
When increased risk has been associated with smok-
ing, no dose response has been seen.^^ Because of
the excessive rates of stomach cancer among south
Louisiana blacks, a case-control study was conducted
concurrently with that of lung cancer utilizing the
same study design and interview.^ A total of 391 cases

TABLE 3

ESTIMATED RELATIVE RISK FOR LUNG CANCER IN
LOUISIANA BY SMOKING CHARACTERISTICS

Number of Adjusted*

Cases Relative Risk

Nonsmokers

1.0

Filter

8.4

Nonfilter

395

15.2

Age started

<16

604

24.2

16-20

515

17.4

21 +

167

8.3

Current smoker

1021

12.6

Quit

3-5 years

7.7

6-20

154

7.0

20 +

100

3.9

Inhalation

None

4.6

Mouth

151

6.3

Chest

1056

11.3

* Adjusted for sex and age

Source: Correa P, Pickle L, Fontham E, et at; The causes of
lung cancer in Louisiana, in Lung Cancer: Causes and Preven-
tion, Mizeil M, Correa P, (eds). Verlag Chemie International,
Deerfield Beach, Fla 1984, p 7^

and matched controls were included. Table 4 presents
estimates of relative risk of stomach cancer associated
with tobacco smoking. Significantly increased risk was
associated with cigar and pipe smoking in whites and
for current cigarette smokers among blacks. No sig-
nificant linear trend in risk was found for number of ^

JOURNAL VOL 140 APRIL 35

TABLE 4

ESTIMATED RELATIVE RISK OF STOMACH CANCER
ACCORDING TO TOBACCO USE

Adjusted Relative
Number of

Smoking Status

Cases

Whites

Blacks

Non-smokers

100

1.0

Cigars and/or

3.61t

2.49

pipe only

Cigarettes only

223

1.28

2.61

Combined types

0.95

1.54

of smokers

Ex-cigarette

1.04

1.85

smokers

Current cigarette

190

1.35

2.66t

smokers

* Adjusted for age, sex, current alcohol consumption, respond-
ent status, education and income
Source; Correa, Fontham, Pickle et al. JNCI 75(4):645-654, 1985.
t p < 0.05, referent non-smokers

cigarettes per day, pack-years or for age at which
smoking began. For blacks only, an increasing risk
was found with increasing duration of smoking. A
significant inhalation effect was found. Deep inhalers
had an estimated relative risk of 1.8 (p < 0.05) com-
pared to non-smokers and non-inhalers.

The failure to find a dose-response in this and
other studies as noted suggests that the association
between tobacco use and stomach cancer is not a causal
one. It is possible that smoking acts as an irritant and
stimulator of acid secretion, facilitating the actions of
other gastric carcinogens.

Pancreas Cancer

Results of the case-control study of pancreatic carci-
noma, the third cancer site in the three-pronged in-
vestigation of excess cancer rates in Louisiana, high-
light cigarette smoking as an important risk factor in
southern Louisiana.®

A significantly increasing risk with increasing cig-
arette dose was seen for both sexes (Table 5). No
excess risk associated with the limited use of other
tobacco products (cigars, pipes, snuff, or chewing to-
bacco) was evident in this study population.

36 JOURNAL VOL 140 APRIL

TABLE 5

ESTIMATED RELATIVE RISK OF PANCREATIC CANCER
AMONG CURRENT SMOKERS BY SEX

Cigarettes
Per Day

Number of
cases

Adjusted
Relative Risk*

Males

Females

Never smokers

122

1.0

1-15

1.31

1.73

16-25

2.02t

1.82

26 +

1.76t

3.66t

* Adjusted for age, respondent status, income, history of dia-
betes mellitus, coffee, alcohol and fruit consumption
t p < 0.05, referent never smokers

Several possible mechanisms of pancreatic car-
cinogenesis by cigarette smoke have been suggested:
the absorbed carcinogens may reach the pancreas
through the blood; inactive carcinogen precursors may
be activated by the liver, excreted into bile, and re-
fluxed from the bile duct to the pancreatic duct; and
finally, smoking may elevate blood lipids, which in
turn, increase the risk of pancreatic cancer.^

Cancers of the Oral Cavity, Cervix, and Bladder

Two studies conducted at Charity Hospital in New
Orleans examined the tobacco-induced cytogenetic
damage in epithelial cells from organs which have
been associated with increased risk of cancer in smok-
ers.

Micronuclei are small fragments of nuclear ma-
terial (DNA) which can be found in the cytoplasm of
some exfoliated human cells. Formation of these mi-
cronuclei is a marker of the extent of recent chro-
mosome breakage, when the cells currently being
sloughed were dividing in the basal layer of epithe-
lium. Micronuclei in exfoliated human cells may be
used as an in vivo marker of carcinogenic exposure.

The first study included 486 patients, each of
whom submitted a specimen from one site only (buc-
cal mucosa, bronchus, urinary bladder, or uterine cer-
vix) and answered a brief questionnaire to determine
tobacco and alcohol history as well as other variables
of interest. Significantly elevated proportions of mi-
cronucleated cells were found for smokers compared
to non-smokers in each of these tissues.

TABLE 6

FREQUENCY OF MICRONUCLEATED CELLS BY SMOKING STATUS AND SPECIMEN TYPE

Mean % micronucleated cells (s.e.)*

Urinary

Uterine

Buccal

Bladder

Cervix

Mucosa

Smokers

0.46 (0.04)

0.50 (0.03)

0.47 (0.03)

(n = 99)

Non-smokers

0.08 (0.01)

0.21 (0.02)

0.08 (0.01)

(n = 101)

p < 0.001 1

p < 0.001

* s.e. = standard error of the mean

t p values from standard t-test, smoker vs. non-smoker

A follow-up study was then conducted in which
exfoliated cells were obtained from multiple sites in
each individual. This study had two purposes: (1) to
confirm the findings of the pilot study of an increased
proportion of micronuclei among cigarette smokers
compared to non-smokers in epithelial cells of the oral
cavity, bladder, and cervix, while controlling for other
known risk factors for cancers of each of these sites;
(2) to examine the magnitude of cytogenetic damage
in tissue from sites which have direct contact with
cigarette smoke, eg, oral cavity, and more distant sites
which do not have direct exposure, such as the blad-
der and the cervix.

The data presented in Table 6 demonstrate to-
bacco-induced chromosome damage in buccal, blad-
der, and cervical tissues consistent with increased risk
of cancer at these sites among smokers. Within the
same individual, the effect was of similar magnitude
in tissue with direct contact and in the more distant
organs. Even after controlling for cervical cancer risk
factors (age at first intercourse, number of sexual part-
ners, history of venereal disease) the strong tobacco
effect on cervical tissue remained, and the findings
support the hypothesis of a causal role of tobacco in
cervical carcinogenesis.

PASSIVE SMOKING

The first reports suggesting that passive or involun-
tary smoking might increase risk of lung cancer in
non-smokers appeared in 1981.^^'^^ The first report of
a significantly increased risk of lung cancer among
non-smokers married to a smoking spouse in a US
population was from Louisiana. A two-fold in-

creased risk was found for non-smoking men and
women married to smokers. The estimated relative
risk of lung cancer Was 1.48 for those whose spouse
smoked 1-40 pack-years and 3.1 for those whose
spouse smoked more than 40 pack-years (p < 0.05).

Most of the studies of passive smoking reported
to date have been based on relatively small numbers
of cases. For example, of the 1,338 lung cancer pa-
tients in the Louisiana study, only 30 (8 men and 22
women) were non-users of tobacco. If the passive
smoking effect is specific for a particular histologic
type as has been suggested by recent work,^^ then
larger sample sizes are needed to estimate risk. It is
critical to include only lifetime non-smokers as cases.
Misclassification of only a small proportion of smok-
ers as non-smokers could elevate the estimate of rel-
ative risk to the levels reported because active smok-
ers have a risk of lung cancer many times greater than
true non-smokers.

In order to study passive smoking in the detail
required to address the unanswered questions, a new
study was initiated in January 1986, centered in the
Dept of Pathology of LSU Medical School. In collab-
oration with researchers in Atlanta, Houston, Los An-
geles, and San Francisco, aU newly diagnosed cases
of primary lung cancer in women are being identified.
The combined population of the study areas is ap-
proximately 15 million persons.

The earlier Louisiana lung cancer study also ex-
amined the association of parental smoking and lung
cancer risk in their adult offspring smokers. This
study did not demonstrate an association between
lung cancer risk and paternal smoking. There was,

JOURNAL VOL 140 APRIL 37

Physicians Recognition Award

Eleven physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
January, 1 988. This award is presented by the American Medical Association to physicians who have voluntarily
completed 150 hours of continuing medical education during a consecutive three-year time period. Of these
150 hours, at least 60 must be in AMA/PRA Category 1. These eleven individuals are presented below.

Alexandria

Alvin Herbert Honigman, MD

Baton Rouge

Tyrone Thomas Girod, MD

Lafayette

Pamela Susan Darr, MD

New Orleans

Ana Maria Comaru-Schally, MD*
Michael Patrick Dolan, MD
Ronald Lee Nichols, MD
Chester Bruno Scrignar, MD
Kenneth Lawrence Veca, MD
Daniel Keith Winstead, MD

Shreveport

Clarence Elmo Boyd, MD
Charles C. Schober, MD

* This individual is not a member of the Louisiana State Medical Society.

The criteria for PRA are planned for maximum compatability with other voluntary or required CME programs.
Physicians who have qualified for CME programs sponsored by the following medical organizations have met
the requirements for the AMA/PRA.

American Academy of Dermatology (AAD)

American Academy of Family Physicians (AAFP)

American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS)
American College of Obstetricians & Gynecologists (ACOG)

American College of Preventive Medicine (ACPM)

American Psychiatric Association (APA)

American Society of Clinical Pathologists/College of American Pathologists (ASCP/CAP)

American Society of Colon & Rectal Surgeons (ASCRS)

American Society of Plastic & Reconstructive Surgeons, Inc. (ASPRS)

American Urological Association, Inc. (AUA)

Arizona Medical Association, Inc. (ArMA)

California Medical Association (CMA)

Medical Society of the District of Columbia (MSDC)

Medical Society of New jersey (MSNj)

Medical Society of Virginia (MSV)

National Medical Association (NMA)

Pennsylvania Medical Society (PMS)

Physicians who have qualified within the last 3 years for the certification program sponsored by CMA, have
met the requirements of AAD, AAFP, or the Continuing Professional Development Program (CPD) of ACOG
may receive the AMA/PRA upon request. Physicians who qualify for the ArMA/CME, and the joint ASCP/CAP
Pathology CME Certificate automatically receive the PRA.

38 JOURNAL VOL 140 APRIL

however, approximately a 40% increased risk of lung
cancer in adult offspring smokers associated with ma-
ternal smoking; and this association persisted after
controlling for variables indicative of active smoking.
These findings indicate that maternal smoking results
in a slight increased lung cancer risk but are not suf-
ficient to determine whether the effect is a result of
enhanced active smoking of the offspring or of in-
creased susceptibility to lung cancer induction after
the challenge of active smoking in later life.

Biologic plausibility of a passive smoke effect in
lung carcinogenesis is supported by laboratory find-
ings. Sidestream smoke (inhaled by nonsmokers)
contains much higher concentrations of toxic and car-
cinogenic compounds than mainstream smoke. Ni-
trosamines (frequently carcinogenic) are especially ex-
! cessive in sidestream smoke. Nicotine metabolites
have been demonstrated in the blood and urine of
adult non-smokers passively exposed to cigarette
smoke; when nitrosated, they are carcinogenic.^^ In
addition, findings from a recently completed study in
New Orleans demonstrated fetal exposure to nicotine,
cotinine (the major metabolite of nicotine) and thio-
cyanate, which is a good indicator of nitrosation po-
tential. This documentation and quantification of del-
eterious components of tobacco smoke in the fetal
environment strengthens the already weighty argu-
ment for smoking cessation during pregnancy.

SMOKELESS TOBACCO

Use of chewing tobacco and snuff among teenagers
appears to be increasing, and this smokeless tobacco
is a major risk factor for cancers of the mouth and
throat.^® These cancers usually develop at the site di-
rectly exposed to tobacco: cigarette smokers develop
more throat cancer and users of snuff and chewing
tobacco more cancers of the gum and buccal mucosa.
A 1986 Consensus Development Conference spon-
sored by the National Institute of Health estimates
that at least 10 million Americans have used smoke-
less tobacco within the past year, including three mil-
lion users under 21 years of age.^® The need to address
this issue is apparent. Mortality rates for white males
throughout the state currently exceed the national
average, and black and white males in the metropol-
itan region of New Orleans have the highest rates in
the state. Increased use of this type of tobacco raises
the concern of increased incidence and mortality

from oral cancer as today's youthful users reach
adulthood. ■

ACKNOWLEDGMENTS

The authors wish to gratefully acknowledge the par-
ticipation of the following institutions in one or more
of the reported studies: Abbeville General Hospital,
American Legion Hospital — Crowley, Baton Rouge
General Hospital, Charity Hospital of New Orleans,
Doctor's Memorial Hospital, East Ascension Parish
Hospital, Houma Medical and Surgical Clinic, Iberia
Parish Hospital, Intercommunity Cancer Center, La-
fayette General Hospital, Lake Charles Memorial
Hospital, Earl K. Long Memorial Hospital, Huey P.
Long Memorial Hospital, Louisiana State University
Hospital, Moosa Memorial Hospital, Dr Walter O.
Moss Regional Hospital, Ochsner Foundation Hos-
pital, Opelousas General Hospital, Our Lady of the
Lake Regional Medical Center, Our Lady of Lourdes
Hospital, Perkins Radiation Center, Rapides General
Hospital, St Francis Cabrini Hospital, St Patrick Hos-
pital, Savoy Memorial Hospital Foundation, Schum-
pert Medical Center, Thibodaux General Hospital,
Touro Infirmary, University Medical Center, Veterans
Administration Hospital — Alexandria, Veterans
Administration Hospital — New Orleans, Veterans
Administration Hospital — Shreveport, Ville Platte
General Hospital, West Calcasieu-Cameron Hospital.

This work was supported by contract No. NOl
CP91023 of the National Cancer Institute and grants
from the American Cancer Society, the Louisiana State
Board of Regents, and the Louisiana Cancer and Lung
Trust Fund Board.

REFERENCES

1. Doll R, Peto R: The Causes of Cancer. New York, Oxford University Press,
1981, p 1256.

2. Cancer Incidence in Five Continents, vol 4. Waterhouse J, Shanmugaratnam
K, Muir C, Powel J, (eds). lARC Sci Pub (42), Lyon, 1982.

3. Correa P, Johnson WD: Cancer and lifestyle in Louisiana. / La State Med
Soc 1983;3:4-6.

4. Correa P, Pickle LW, Fontham E, et al: The causes of lung cancer in
Louisiana, in Lung Cancer Causes and Prevention. Deerfield Beach, Fla,
Verlag Chemie International, 1984, pp 73-82.

5. Kahn HA: The Dom study of smoking and mortality among US veterans:
Report of 8V2 years of observation. Natl Cancer InstMonogr 1961;19:1-126.

6. Hirayama T: Epidemiology of stomach cancer. Jpn J Cancer Res 1971;11:3-
19.

7. Correa P, Fontham E, Pickle LW, et al: Dietary determinants of gastric
cancer in south Louisiana. }NCI 1985;75:645-653.

8. Falk R, Pickle LW, Correa P, et al: Lifestyle risk factors for pancreatic
cancer. Am } Epidemiol 1986;124:502.

9. Wynder EL: Ajn epidemiological evaluation of the causes of cancer of
the pancreas. Cancer Res 1975;35:2228.

JOURNAL VOL 140 APRIL 39

specify Adjunctive

10. Fontham E, Correa P, Rodriguez E, et al: Validation of smoking history
with the micronuclei test, in Banbury Report 23: Mechanisms in Tobacco
Carcinogenesis. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY,
1986, pp 113-119.

11. Hirayama T: Nonsmoking wives of heavy smokers have a higher risk of
lung cancer: A study from Japan. Br Med } [Clin Res] 1981;282:183-185.

12. Trichopolos D, Kalandidi A, Sparros L, et al: Lung cancer and passive
smoking. Int ] Cancer 1981;27:1-4.

13. Correa P, Pickle LW, Fontham EH, et al: Passive smoking and lung
cancer. Lancet 1983;2:595-597.

14. Dalager MA, Pickle LW, Correa P, et al: Passive smoking and lung cancer
among non-tobacco users. Cancer Res 1986;46:4808-4811.

15. Correa P: The passive smoking-cancer controversy, in Banbury Report 23:
Mechanisms in Tobacco Carcinogenesis. Cold Spring Harbor Laboratory,
Cold Spring Harbor, NY, 1986, pp 343-360.

16. Weiss ST, Tager IB, Schenker M, et al: The health effects of involuntary
smoking. Am Rev Respir Dis 1983;128:933-942.

17. Hoffman D, Hecht SS: Nicotine-derived N-nitrosamines and tobacco-
related cancer: Current status and future directions. Cancer Res 1985;45:935-
944.

18. National Institutes of Health consensus development conference state-
ment: Health implicahons of smokeless tobacco use. CA 1986;36(5):310-
316.

19. Smith EM: Epidemiology of oral and pharyngeal cancers in the US:
Review of recent Literature. / Natl Cancer Inst 1979;63:1189-1198.

Drs Fontham, Correa, and Chen are from the Dept of Pathology at LSU

Medical Center in New Orleans.

Ms Craig is from the Louisiana Tumor Registry in the Dept of Health
and Human Resources in New Orleans.

Drs Pickle and Falk are from the Environmental Epidemiology Branch
of the National Cancer Institute, in Bethesda, MD.

Reprint requests should be sent to Elizabeth Fontham, MD,
Dept of Pathology, LSU Medical Center, 1901 Perdido St,

New Orleans, LA 70112.

40 JOURNAL VOL 140 APRIL

(Hit)

/TCP

Each capsule contains 5 mg chlordiazepoxide HCl and 2.5 mg
clidinium bromide

Please consult complete prescribing information, a summary of which
follows:

Indications: Based on a review of this drug by the National Acad-
emy of Sciences— National Research Council and/or other informa-
tion, FDA has classified the indications as follows:

“Possibly” effeaive: as adjunctive therapy in the treatment of peptic
ulcer and in the treatment of the irritable bowel syndrome (irntable
colon, spastic colon, mucous colitis) and acute enterocolitis.

Final classification of the less-than-effective indications requires fur-
ther investigation.

Contraindications: Glaucoma; prostatic hypertrophy, benim bladder
neck obstruction; hypersensitivity to chlordiazepoxide HCl and/or
clidinium Br.

Warnings: Caution patients about possible combined effects with alco-
hol and other CNS depressants, and against hazardous occupations
requiring complete mental alertness {e.g., operating machinery, driving).
Physical and psychological dependence rarely reported on recommended
doses, but use caution in administering Librium® (chlordiazepoxide HCl/
Roche) to known addiction-prone individuals or those who might
increase dosage; withdrawal symptoms (including convulsions) reported
following discontinuation of tne drug.

Usage in Pregnancy: Use of minor tranauilizers during first
trimester should almost always be avoided because of uicreased
risk of congenital malformations as suggested in several studies.
Consider possibility of premancy when instituting therapy.

Advise patients to discuss therapy if they intend to or do
become pregnant.

As with all anticholinergics, inhibition of lactation may occur.

Precautions: In elderly and debilitated, limit dosage to smallest effective
amount to preclude ataxia, oversedation, confusion (no more than
2 capsules/aay initially; increase gradually as needed and tolerated).
Though generally not recommended, if combination therapy with other
psychotropics seems indicated, carefully consider pharmacology of
agents, particularly potentiating drugs such as MAO inhibitors, pheno-
thiazines. Observe usual precautions in presence of impaired renal or
hepatic funaion. Paradoxical reactions reported in psychiatric patients.
Employ usual precautions in treating anxiety states with evidence of
impending depression; suicidal tendencies may be present and protective
measures necessary. Variable effects on blood coagulation reported very
rarely in patients receiving the drug and oral anticoagulants; causal rela-
tionship not established.

Adverse Reactions: No side effects or manifestations not seen with
either compound alone reported with Librax. When chlordiazepoxide HCl
is used alone, drowsiness, ataxia, confusion may occur, especially
in elderly and debilitated; avoidable in most cases by proper dosage
adjustment, but also occasionally observed at lower dosage ranges. Syn-
cope reported in a few instances. Also encountered: isolated instances of
skin eruptions, edema, minor menstrual irregularities, nausea and con-
stipation, extrapyramidal symptoms, increased and decreased libido —
all infrequent, generally controlled with dosage reduction; changes in
EEG patterns may appear during and after treatment; blood dyscrasias
(including agranulocytosis), jaundice, hepatic dysfunction reported
occasionally with chlordiazepoxide FICI, making periodic blood counts
and liver function tests advisable during protracted therapy. Adverse
effects reported with Librax typical of anticholinergic agents, i.e., dry-
ness of mouth, blurring of vision, urinary hesitancy, constipation. Con-
stipation has occurred most often when Librax therapy is combined
with other spasmolytics and/or low residue diets.

Roche Products Inc.
Manati, Puerto Rico 00701

PI. 0186

DIET, NUTRITION, AND CANCER

PELAYO CORREA, MD; ELIZABETH FONTHAM, DPH;
VIVIEN CHEN, PhD; JEAN F. CRAIG, MS; RONI FALK, MS;

LINDA W. PICKLE, PhD

Results of three case-control studies of cancer in
Louisiana are presented, addressing dietary and
nutritional factors related to cancers of the
stomach, pancreas, and lung. Smoked and cured
meats and excessive use of salt were found
associated with an increased risk of gastric cancer.
Pork products were associated with an increased
risk of pancreatic cancer. A common finding for
cancers of the stomach, pancreas, and lung is that
fresh fruits and fresh vegetables, as well as
vitamin C and beta-carotene, appear to exert a

protective effect.

T he role of diet and nutrition in cancer causation
in general is being emphasized, mostly because a
wealth of recent studies have uncovered previously
unsuspected interrelationships, summarized in a
comprehensive review by the National Academy of
Sciences.^

Louisiana offers a special opportunity to study
the diet-cancer relationship because of the unique set-
ting provided by the different racial and cultural pop-
ulation groups (Cajuns, Scotch-Irish, blacks, etc),
which have preserved their own dietary patterns. We
have recently conducted a series of epidemiologic
studies which have provided information of interest
in this area. They were carried out thanks to the ex-
cellent collaboration of the physicians of Louisiana
who allowed us to interview more than 3,000 of their
patients to obtain dietary information. The authors
consider the publication of the results a tribute to the
Louisiana physicians who have made this research
possible. The findings are here summarized and dis-
cussed in the light of cultural idiosyncrasy of dietary
habits in Louisiana.

JOURNAL VOL 140 APRIL 43

LOUISIANA POPULATION

Both cancer and diet are markedly influenced by cul-
ture, and a few words about the Louisiana population
are in order. Culturally, there is more than one Lou-
isiana. Prominent local sociologists who have studied
the subject extensively distinguish coastal Louisiana
from non-coastal Louisiana.^ The former is composed
of 29 parishes covering 42% of the territory and 67%
of the population, with four major urban centers, and
a younger population structure. It was settled mostly
by French-Canadians (welcomed by the then Spanish
government of the state), who were predominantly
Catholic and not too committed to birth control prac-
tices, and who became "water-oriented" for food,
livelihood and transportation. This contrasts with non-
coastal Louisiana, mostly rural and Protestant, more
inclined to practice birth control, settled by descen-
dants of Anglo-Saxon, Scotch-Irish, and other non-
French Europeans, with an agricultural structure in-
fluenced by land holding patterns prevalent in an-
tebellum times. Then there is the black Louisiana with
its own cultural characteristics but also interacting in
different ways with the coastal and non-coastal white
populations, and in both cases predominantly occu-
pying lower socioeconomic strata, having an African-
type of population structure with a high dependency
index (ratio of children to working adults).^ The high-
est proportions of black population and of families
below poverty level are concentrated in non-coastal
Louisiana and especially along the west bank of the
Mississippi River. ^

DIET IN LOUISIANA

Marked differences of dietary patterns in coastal ver-
sus non-coastal whites and blacks have been re-
ported. The eating pattern is very complex, influ-
enced in each subgroup to different degrees by
accessibility, family needs, and social prestige of
foods. ^ Typically, north Louisiana whites report higher
consumption of miscellaneous vegetables, potatoes,
and miscellaneous fruits when compared to other
groups. South Louisiana whites prefer fish, seafood,
and salads more than other groups. Blacks prefer pork
meats, cornbread and rice. The diet seems more var-
ied in the north than in the south in both races but
especially in whites. Northern whites drink tea and
citrus fruits while southern whites prefer beer. Blacks

prefer soft drinks. Many other differences have been
reported by the scholarly work of Steelman which was
published more than a decade ago.^ No recent similar
reports are known to the authors by which to assess
changes that may have taken place since then in each
of the four sociocultural groups. But the data of Steel-
man as of 1974 provide a rational base to study the
influence of diet on cancer in these subcultures. This
is particularly relevant if we consider that cancer rates
at the present time are influenced by exposures ex-
perienced years before because of the prolonged la-
tency of the carcinogenesis process. We published in
this journal the results of a survey of adult males in
north and south Louisiana (non-Cajuns versus Ca-
juns) which emphasizes the geographic and racial dif-
ferences in diet, including alcohol use.^

NUTRITION IN LOUISIANA

Diet provides nutrients and non-nutrient compo-
nents, both of which are important in cancer etiology.
Several national nutritional surveys have included
Louisiana, but few results specific for Louisiana sub-
populations have been analyzed and published.

Dietary intakes and biochemical indices of nutri-
tional status in a sample of Louisiana residents were
obtained during the Ten-State Nutrition Survey, 1968-
1970.^ Mean intake and serum levels of retinol and
beta-carotene for black and white men 18 years and
older were calculated for 19 parishes. The approxi-
mate intake in the northern parishes was 5,886 lU of
vitamin A activity while the corresponding intake for
the south was 2,526 lU — less than one half. Serum
levels of vitamin C were deficient and low in 15% of
low income and 9% of higher income Louisiana res-
idents. A strong negative correlation between serum
levels of beta-carotene and vitamin C and lung cancer
mortality rates has been reported.^

The Bogalusa Heart Study is an epidemiologic
investigation of the early natural history of coronary
artery disease and hypertension in a biracial pediatric
population.® As part of this study, vitamin intakes
were determined in 10 and 13-year-old children. In
four sex-race groups, 25% to 50% of the children sur-
veyed did not consume the recommended daily al-
lowance (RDA) of vitamin A, thiamine, and ribo-
flavin. Among the children who never took
supplemental vitamins, 15% to 36% had dietary in-
take of vitamin C less than one-third of the RDA. The

44 JOURNAL VOL 140 APRIL

Whites
Odds Ratio

Blacks
Odds Ratio

Food items

Pork

1.44

1.35

Rice

1.34

1.35

Corn bread

1.32

1.57

Candy

0.90

2.12*

Cake

1.00

1.56

Coffee

1.79

0.90

Salt

1.17

1.34

Lettuce

0.72

0.52

Tomato

0.82

0.56

Banana

0.73

0.61

Orange

0.69

0.89

Fruit juice

0.74

0.47

Broccoli

1.04

0.50

Food groups

Pork products

1.68*

1.42

Carbohydrates

1.43

0.76

Sweets

0.98

1.88*

Vegetables

0.90

0.70

Fruits

0.66

0.65

Vitamin indexes

Vitamin C

0.62*

0.63

Carotenoids

0.68

1.08

Total vitamin A

1.22

0.85

children who most needed an ascorbic acid supple-
ment were the least likely to take one. These findings
for children and adolescents parallel those for Loui-
siana adults in the sirrveys noted and suggest that
the problem of low intake of key micronutrients is
culturally determined at an early age.

STOMACH CANCER

Marked changes in the frequency of gastric cancer
have been observed in Louisiana. Around 1950, whites
and blacks in the southern portion of the state had
rates above the national average. The excess was then
shared with the north central and Rocky Mountain
states.^ A decade later, the excess in south Louisiana
had totally disappeared in whites but persisted in
blacks.^® There is scientific consensus in assigning diet

as the overriding cause of gastric cancer, which should
lead to the conclusion that dietary changes have oc-
curred in south Louisiana which have eliminated the
gastric cancer excess in whites but not in their black
counterparts — an interesting subject for further re-
search. The rates are also declining in blacks, but since
the rates in south Louisiana blacks are stiU higher than
those of other blacks in the country, it may be spec-
ulated that the Cajun influence in their cooking habits
may be related to stomach cancer.

A case-control study was conducted recently in
which 391 patients with gastric cancer or their next-
of-kin were interviewed (126 white males, 68 white
females, 138 black males and 59 black females). A
similar number of controls matched by sex, age, and
race were also interviewed. The study covered 26 par-
ishes in south Louisiana. The patients were diag-
nosed, between January 1979 and March 1983, as hav-
ing gastric carcinoma. A food frequency questionnaire
including 59 items was administered, emphasizing
dietary habits prior to the illness under study.

A brief summary of the dietary determinants of
risk is shown in Table 1 in terms of odds ratios (OR),
which approximate the relative risk (RR) associated
with each factor, given a baseline of 1.0 to indicate
lack of effect.

In addition to the findings shown, consumption
of smoked foods (RR 1.70) and home made sausages
or home cured meats (RR 2.32) were associated with
significant increases in the risk of stomach cancer in
blacks.

Alcohol intake was also associated with greater
cancer risk; the stomach cancer relative risk for current
drinkers was 1.49 in whites and 1.66 in blacks. The
consumption of fresh fruits and vegetables was in-
versely related to the risk in whites and blacks of
south Louisiana. A dose-response pattern was ob-
served for vitamin C intake: those in the highest quar-
tile of consumption had a decreased risk (OR 0.33 in
whites and 0.50 in blacks), suggesting a rather strong
protection by this vitamin. The effect of carotenoids
disappeared when vitamin C was controlled, but the
effect of vitamin C remained after controlling for other
risk factors, including carotenoid intake.

Salt intake is a known risk factor of stomach can-
cer, and excessive salt intake appears to be a char-
acteristic of south Louisiana diet. Accurate measures
of salt intake are cumbersome and not frequently at-
tempted. Houston blacks use more salt than whites,^^

JOURNAL VOL 140 APRIL 45

TABLE 2

SIGNIFICANT* DIETARY DIFFERENCES BETWEEN BLACKS
AND WHITES IN SOUTH LOUISIANA

Consumption higher in whites

Consumption higher
in biacks

Shrimp

Carrots

Fish

Oysters

Eggplant

Eggs

Crabs

Green Beans

Red Beans

Crawfish

Corn

White beans

Clams

Lima beans

Rice

Scallops

Bananas

Corn Bread

Milk

Strawberries

Spinach

Cheese

Other fruits

Sweet potatoes

Potatoes

Canned fruits

Greens

Pasta

Preserves

Okra

Cereal

Potato chips

Fruit juice

Bread

Fritos

Chicken

Broccoli

Popcorn

Sausage

Cabbage

Cakes and pies

Cold cuts

Lettuce

Beef

Organ meats

Squash
Tomatoes
Brussel sprouts

Ham

Fresh pork

* p < .05 determined by Wilcoxon rank sum test.

and excessive salting of foods by blacks is a common
observation in Louisiana (again, not scientifically doc-
umented). In our study, adding salt to food on the
table was associated with a risk to 1.36 in whites and
1.75 in blacks. Although not statistically significant,
these observations are in the expected direction, as
indicated by other studies.

The pattern emerging from this study suggests
that diet is the main determinant of gastric cancer risk
in south Louisiana. Food items associated with in-
creased risk include some that are very popular in the
region, such as pork meats, smoked meats, home-
cured meats and sausage, rice, and corn bread. Other
popular Louisiana food items, such as crawfish, oys-
ters, shrimp, and crabs, did not show any effect on
gastric cancer risk. Items associated with lower risk
consistently fell in the category of fresh fruits and
fresh vegetables.

The high risk of gastric cancer in south Louisiana
is limited to blacks. This finding led to a comparison
of the dietary patterns of blacks and whites. The com-

parison was achieved by pooling the data for controls
in three large case-control studies (lung, pancreas,
and stomach) that had been conducted simultane-
ously in south Louisiana. The results, summarized in
Table 2, were based on interviews with 1,332 white
and 686 black residents of south Louisiana. Statisti-
cally significant black- white differences (p < 0.05) in
the frequency distributions of consumption are pre-
sented. The comparisons agree with our findings for
the relative risks: whites (the population at lower risk)
consume more vegetables, salad greens, fresh fruits
and dairy products, whereas the blacks (the popu-
lation at higher risk), consume more grains and starchy
foods. There also are differences in the sources of
animal proteins and fat. Blacks have a higher con-
sumption of legumes and nitrite-preserved meats, such
as sausage and cold cuts. Possibly, economic reasons
influence these food patterns inasmuch as the foods
preferred by whites are generally more expensive.
This possibility is consistent with the well-known in-
verse correlation between economic status and gastric
cancer risk and perhaps with the time trends of death
rates for both races in south Louisiana.

In conclusion, the high gastric cancer rates in
south Louisiana, especially in blacks, may be linked
to the effects of economy and traditional dietary pat-
terns. Increased risk is mostly associated with smoked
or home-cured meats, alcohol, and probably excessive
salt intake. Lower gastric cancer risk is primarily as-
sociated with fresh fruits and vegetables with their
high content of vitamin C and carotenoids. A separate
study of chronic atrophic gastritis in New Orleans
blacks again showed a very strong inverse association
with intake of vitamin C and fresh fruits and vege-
tables.^^ Chronic atrophic gastritis is considered a pre-
cursor of gastric carcinoma. Changes taking place in
dietary habits are likely to be responsible for the de-
cline in rates observed in recent decades. The above
findings may offer opportunities to accelerate this de-
cline, especially in populations at highest risk, namely
the blacks of coastal Louisiana.

PANCREATIC CANCER

County-specific cancer maps for 1950-1969 in the
United States showed little geographic variation ex-
cept for a cluster of parishes with high rates in south-
ern Louisiana, particularly among white males.^° Of
the 64 parishes of Louisiana, 25 had death rates for

46 JOURNAL VOL 140 APRIL

TABLE 3

ADJUSTED ODDS RATIOS FOR PANCREATIC CANCER

Male Female

Servings/Month Odds Ratio Odds Ratio

Breads and Cereals
<32
32-59
60 +

Beef
<6
6-15
16 +

Pork Products
<9
9-30
31 +

Seafood
<2
2-7
8 +

Dairy
<34
34-67
68 +

Rice
<4
4-29
30 +

Fruits/Juices
<25
25-63
64 +

Vegetables
<32
32-73
74 +

Vitamin Ct
<2000
2000-4455
4456*

Vitamin A§

<18680

18680-43577

43578*

Retinoi§

<11872

11872-35631

35632*

Carotene§

<4436

4436-9347

9348*

* p <0.05

t Test for trend p <0.05

t Expressed as milligrams per month

§ Expressed as the number of retinoi equivaients per month

pancreatic cancer in the top 10% of all US counties
for white males and 10 had rates in the top 10% for
black males. More recent mortality maps for the 70s
showed persistently high rates in south Louisiana.

Simultaneously with the gastric cancer study re-
ferred to above and utilizing the same methodology,
we interviewed 363 cases of pancreatic cancer and
compared their responses to those of 1,234 subjects
originally identified as controls for the pancreas,
stomach, and lung cancer cases. Details of the study
design and methodology are given in a separate pub-
lication.^^

Table 3 summarizes the findings with respect to
diet and nutrition, presented as odds ratios adjusted
for age, cigarette smoking, income, residency, history
of diabetes, Cajun ethnicity, and respondent status
to avoid confounding by these factors.

Elevated risks associated with frequent con-
sumption of bread and cereal, pork products, and rice
were found. Fruit consumption showed a significant
inverse association. The risk for persons reporting
high dietary intake of vitamin C was 38% of the risk
associated with low intake in males and 55% in fe-
males. No significant effect was found for alcohol or
coffee drinking.

A study of food interactions revealed an inverse
correlation between fruit and pork intake. High fruit
intake diminished the risk associated with pork con-
sumption while low fruit and juice consumers dis-
played significantly increased risk associated with pork
intake. Heavy coffee drinkers were very low con-
sumers of fruits, and an elevated risk of pancreatic
cancer among heavy coffee drinkers was seen only in
low consumers of fruit. This may be considered in
evaluating reports of elevated risk of pancreatic cancer
in heavy coffee drinkers in studies in which the con-
sumption of fruit was not adequately evaluated.

The influence of ethnicity was clear for some
items. Cajuns tend to eat fewer fruits and more rice
than non-Cajuns. A strong trend of increasing risk
for pork products emerged among Cajuns only. The
effect of vitamin C was stronger among Cajuns.

Our findings concerning the antagonistic effects
of pork products and fruits are similar for stomach
and pancreatic cancer. This suggests similarities in the
carcinogenesis process of both types of tumors. We
have previously suggested intragastric nitrosation, and
its blockage by vitamin C, as a possible etiologic model
for gastric cancer.

1.00

1.52*

1.15

1.26

1.28

1.00

1.19

0.83

1.08

0.70

1.00

1.39

1.58

1.72t

1.26

1.00

0.98

1.22

1.00

1.87t

1.00

1.55

1.61

2.18*t

0.97

1.00

0.94

1.21

1.46

1.16

1.00

0.62*

0.58

0.40*t

0.46*t

1.00

1.36

1.09

1.25

1.33

1.00

0.53*

0.77

0.38*t

0.55t

1.00

1.36

1.09

1.55

1.13

1.00

1.48

0.94

1.57t

0.85

1.00

0.99

1.26

0.82

1.65

JOURNAL VOL 140 APRIL 47

TABLE 4

ADJUSTED RELATIVE RISK OF LUNG CANCER ASSOCIATED WITH ABOVE-MEDIAN
CONSUMPTION OF SELECTED FOOD GROUPS

All Lung

Squamous &

Cancers

Small Cell

Adenocarcinoma

Dairy Products

0.90

0.80

Pork products

1.04

1.30

Nitrite meats

1.03

1.01

1.12

All meats

0.90

0.98

0.97

Seafoods

0.93

0.86

1.27

Breads, grains & cereals

1.04

1.25

0.70

Vegetables

0.79*

0.70*

Fruits

0.77*

0.73*

1.00

Fruits & vegetables

0.68*

0.72*

* p < .05

LUNG CANCER

The excess of lung cancer in south Louisiana has been
amply documented. The monographs of the Loui-
siana Tumor Registry have reported on incidence and
mortality rates, time trends, and differences by age,
sex, and geographic location.^ It has been estimated
that lung cancer accounts for 85% of the excess of
cancer in Louisiana when compared to the United
States.

As explained above, we conducted a case-control
study in south Louisiana simultaneously for cancers
of the lung, stomach, and pancreas. Interviews with
1,253 lung cancer patients and 1,274 controls yielded
data on diet and nutrition summarized below. Table
4 shows the findings for selected food groups by his-
tologic type, adjusted for race, sex, age, cigarette use,
family income, ethnic group, and respondent status
in order to avoid confounding of the results by these
variables. As seen in the table, the only food groups
affecting significantly the risk of lung cancer are fruits
and vegetables, which are associated with a lower
risk. Analysis of the nutrient content of food revealed
a significant effect of vitamin C and carotene for squa-
mous and small cell carcinomas but not for adeno-
carcinoma. Surprisingly, lower risk associated with
retinol intake was found only for adenocarcinoma and
was particularly noteworthy among blacks.

The effects of carotene and vitamin C are found
for ex-smokers and current light smokers, but not for

48 JOURNAL VOL 140 APRIL

heavy smokers or lifetime non-smokers. The retinol
effect on adenocarcinoma was most pronounced for
current heavy smokers but its significance is some-
what compromised by the fact that the index was
heavily dependent on the intake of organ meats, and
other factors associated with such food items may be
confounding the retinol effect (unpublished data).

Vitamin C intake adjusted for carotene intake re-
mains a risk-reducing factor, but carotene adjusted
for vitamin C consumption loses its protective effect.
The same results were observed for gastric cancer. It,
therefore, seems that vitamin C may be the most
prominent nutritional factor in the Louisiana popu-
lation (unpublished data).

CONCLUSIONS

1. Historical facts have resulted in the presence of
distinct ethnic and geographical dietary patterns
in Louisiana.

2. These dietary patterns may have an influence in
the peculiar cancer profile of Louisiana, especially
as it relates to high rates of respiratory and diges-
tive tract neoplasms.

3. Dietary items associated with high cancer risk in
south Louisiana are pork meats, smoked and home-
cured meats, rice and corn bread. Excessive salt
intake is suspected as a factor in the high gastric
cancer rates in blacks.

4. Perhaps the most interesting and potentially im-

portant finding is that the Louisiana diet may be
less than optimal in its supply of substances that
may protect against cancer development. The most
prominent nutrient in this regard is vitairiin C,
which may be of special importance to Louisiana's
population. Scurvy is not a frequent disease in
Louisiana, which illustrates the point that the rec-
ommended daily allowance (supposedly sufficient
to prevent scurvy) is not the best measure of the
adequacy of a nutrient in the community. Sub-
optimal carotene intake may also be a prominent
factor related to the high cancer rates of Louisiana.

■

ACKNOWLEDGMENTS

This work was supported by contract No. NOl

CP91023 and Grant No. 28842 of the Etiology Branch

National Cancer Institute.

REFERENCES

1. Diet, nutrition, and cancer. National Research Council. National Academy
Press, 1982.

2. Paterson KW, Lindsey JL, Bertrand AL: The Human Dimension of Coastal
Zone Development, bulletin No. 679. Baton Rouge, La, Louisiana State
University Center for Agricultural Sciences and Rural Development, 1974.

3. Cancer in Louisiana, vol 1 (1983), 2 (1985) and 3 (1986). New Orleans, La,
Louisiana Tumor Registry, Dept of Health and Hmnan Resources, Di-
vision of Administration and Louisiana State University Graphic Serv-
ices.

4. Steelman VP: The Cultural Context of Food: A Study of Food Habits and Their
Social Significance in Selected Areas of Louisiana, bulletin No. 679. Baton
Rouge, La, Louisiana State University Center for Agricultural Sciences
and Rmal Development, 1974.

5. Correa P, Johnson WD: Cancer and lifestyle in Louisiana. J La State Med
Soc 1983;3:4-6.

6. Ten-state Nutritive Survey 1968-1970, 72-8129, 72-8130, 72-8131, 72-8132,
72-8133. US Dept of Health, Education and Welfare, 1972.

7. Lopez A, Yates B, Johnson WD, et al: The role of vitamin A and ascorbic
add in relation to respirator}' system cancers. Abstracted, Am J Clin Nutr
1979;32:954.

8. Farris RP, Cresanta JL, Webber LS, et al: Dietary studies of children from
a biradal population: Intake of vitamins in 1(1- and 13-year-olds. J Am
Coll Nutr 1985;4:539-552.

9. Haerrszel W: Variation in inddence and mortality from stomach cancer
with particular reference to the Uruted States. JNCI 1958,21:213-262.

10. Mason TJ, McKay FW, Hoover R, et al: Atlas of Cancer Mortality for U.S.
Counties: 1950-1969. Washington, DC, Government Printing Office, 1975.

11. Kerr GR, Amante P, Decker M, et al: Ethnic patterns of salt purchase in
Houston, Texas. Am J Epidemiol 1982;115:906-916.

12. Correa P, Fontham E, Williams PL, et al: Dietary determinants of gastric
cancer in south Louisiana. JNCI 1985;75:645-654.

13. Fontham E, Zavala D, Correa P, et al: Diet and chronic atrophic gastritis:
A case-control study. JNCI 1986;76(4):621-627.

14. Falk R, William PL, Fontham E, et al: Lifestyle factors for pancreatic
cancer in Louisiana. Am J Epidemiol, to be published.

Drs Correa, Fontham, and Chen are from the Dept of Pathology at LSU

Medical Center in New Orleans.

Dr Craig is from the Jjouisiana Tumor Registry in the Dept of Health
and Human Resources in New Orleans.

Drs Falk and Pickle are from the Environmental Epidemiology Branch
of the National Cancer Institute in Bethesda, MD.

Reprint requests should be sent to Pelayo Correa, MD, Dept of
Pathology, LSU Medical Center, 1901 Perdido Street,
New Orleans, LA 70012.

JOURNAL VOL 140 APRIL 49

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To find out about the benefits of
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military health care. It’s a flexi-
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participate in a variety of
programs that can put you in
contact with medical leaders
from all over the country.

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be, call our Army Medical
Personnel Counselor.

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LOUISIANA TUMOR REGISTRY

JEAN FIKE CRAIG, MS; VIVIEN W. CHEN, PhD;
PELAYO CORREA, MD; ELIZABETH T.H. FONTHAM, DPH

As a population-based registry^ the Louisiana
Tumor Registry (LTR) provides resources to
combat the serious cancer problem in Louisiana. In
1988 the Registry completed its expansion and now
covers the state. Using a regional registry system,
the LTR is available to provide research
collaboration as well as assessments of the cancer
problem in the state. In addition, the LTR assists
in planning health care services for a specific
geographic area and in implementing hospital

tumor registries.

A bielatively new resource for cancer prevention
and control is available to Louisiana's health care
community — a statewide population-based tumor
registry.

The Louisiana Tumor Registry (LTR) was first
established in 1974 by Charity Hospital as a popula-
tion-based registry for the New Orleans area and as
a participant in the Surveillance, Epidemiology and
End Results (SEER) program of the National Cancer
Institute (NCI). LTR was transferred to the State Of-
fice of Health in 1979 as a pilot for a statewide registry;
federal funding ceased in 1980. Presently, LTR is op-
erated under the Department of Health and Human
Resources (DHHR) umbrella in the Office of Preven-
tive and Public Health Services. Funding for the reg-
istry is provided from the proceeds of a state cigarette
tax dedicated to cancer research. Since 1983, LTR has
gradually expanded region by region until coverage
of the entire state was achieved in 1988.

Policies for the LTR are set by the Louisiana Can-
cer and Lung Trust Fund Board. The 11 members of
the Board represent various health institutions and
are appointed by the governor. The operations of the ►

JOURNAL VOL 140 APRIL 51

registry are mandated by public law, RS 40:1299.80 et
seq, which directs hospitals and pathology laborato-
ries to report their cancer cases to the registry so that
the frequency of cancer in the state can be monitored.
This same law mandates strict confidentiality of the
data, a requirement meticulously observed by LTR
personnel. In the 14 years of operation, not a single
incident compromising the confidentiality of the in-
formation gathered has occurred. The law also grants
to all participating institutions immunity from any
liability which may arise from their reporting of cases
to the registry.

OPERATIONS

In order to compile statistics on the frequency and
types of cancer within defined geographic areas, the
LTR collects information from various departments of
all hospitals in those areas, including medical records,
pathology, radiology, and hematology. In addition,
cases are identified from free-standing pathology lab-
oratories and radiation centers, one-day surgery fa-
cilities, private physicians' offices, coroners' offices,
and the state mortality file. To ensure accuracy in
calculating incidence rates, cancers occurring among
residents who are diagnosed and/or treated outside
the geographic area are also included and all duplicate
reports of cases are collated into one record. Non-
resident cases are excluded in incidence computa-
tions.

In order to have an efficient statewide popula-
tion-based registry, the LTR uses a regional registry
system to collect data from all parishes. The regional
tumor registries are: Baton Rouge Regional Tumor
Registry, Acadiana Tumor Registry, Southwest Lou-
isiana Regional Tumor Registry, Northeast Louisiana
Regional Tumor Registry, Regional Tumor Registry
for Northwest Louisiana, and the Alexandria-area Re-
gional Tumor Registry. The regional registries coor-
dinate the collection of cancer data on residents of
their own regions from all sources and submit them
to the central office in New Orleans. They are re-
sponsible for performing quality control in their re-
gions and ensuring complete coverage. The regional
registries also provide training to hospital staff and
collect follow-up information.

SERVICES PROVIDED

While most physicians are familiar with hospital-based
52 JOURNAL VOL 140 APRIL

tumor registries and the services they offer, many are
not aware of the role of population-based tumor reg-
istries.

The primary concern of a population-based tu-
mor registry is to monitor the frequency of cancer in
the community. Services provided by the LTR to Lou-
isiana residents include:

1. Assessment of the cancer problem. Age-specific
and age-adjusted incidence and mortality rates are
calculated by the LTR using population statistics from
the Census Bureau along with incidence data and
Louisiana Vital Statistics information. These rates can
be compared with national rates and rates of other
states and even other countries to assess the magni-
tude of the cancer problem in Louisiana. In addition,
unusually high-risk or low-risk groups and geo-
graphic clusters of cases can be identified.

As a population-based registry, the LTR also
monitors trends in cancer incidence and mortality.
The data base already established permits detection
of changes in cancer patterns within the state and can
be used to assess the effectiveness of cancer programs
in the community. For example, a shift to an earlier
stage of disease at diagnosis may be the result of a
successful screening program and a decline in mor-
tality may reflect advances in clinical management.

2. Research collaboration. The collaboration of a
population-based tumor registry has been a prereq-
uisite for many NCI epidemiologic research grants.
The LTR is a participant in an on-going epidemiologic
study of black/white differences in cancer patient sur-
vival experience conducted by Louisiana State Uni-
versity Medical School in collaboration with NCI. In
a recent Louisiana project, the LTR has collaborated
with a Lake Charles environmental group, CLEAN,
to investigate cancer in Calcasieu Parish. As a member
of the International Association of Cancer Registries,
the LTR participates in various research projects and
reports its rates for publication in Cancer Incidence in
Five Continents, the most prestigious publication on
cancer incidence.

3. Other services and requests. Other services of the
LTR are provided upon request. Cancer statistics and
reports using aggregate data are available at no charge.
When identifying data are requested, the LTR serves
only as an intermediary, notifying the hospital of the
request and relaying the response to the researcher.
All identifying information, including hospital and

! physician, are confidential and procedures to ensure
; confidentiality are strictly maintained. While reports
lean be prepared comparing one hospital to the rest
! of the hospitals in a geographic area, only data from
the requesting hospital can be identified separately,
i Information identifying specific hospitals cannot be
released to other facilities.

The LTR has library resources of specialized can-
cer epidemiological information. It also offers assist-
ance by suggesting bibliographic references by tele-
phone. Speakers are available to discuss cancer in
Louisiana: its epidemiology, trends and comparisons
with the national rates. Students and the press, as
weU as physicians, are frequent requestors of infor-
mation on cancer in Louisiana.

In addition, the LTR provides consultation and
assistance in the plarming and implementation of both
regional and hospital tumor registries. It also assists
in planning the health care services in a specific geo-
graphic area. By utilizing LTR-computerized infor-
mation, marketing departments of hospitals and other
health care institutions can determine the needs and
demands for utilizing certain equipment or facilities
I for cancer patients.

PUBLICATIONS AND HIGHLIGHTS

The LTR publishes numerous reports among which
are Cancer in Louisiana (published annually) and data
for inclusion in Cancer Incidence in Five Continents. A
few highlights from these publicaitons are listed be-
low:

• Excess cancer mortality for the oral cavity and lung
has been observed in Louisiana males since 1930.^

• For the decade of the 70s, Louisiana ranked first in
lung cancer mortality among white males, 25%
higher than the national rate.^

• During the period 1974-1977, New Orleans white
males experienced the highest risk for lung cancer
among all SEER participants; the incidence rate was
40% higher than the SEER rate.^

• New Orleans black males have the highest inci-
dence rate for lung cancer ever reported world-
wide.^

• White females in Louisiana were foimd to have lower
mortality rates for most cancer sites when compared
to the national averages. Similarly, lower incidence
rates for most cancers were observed for white fe-
males in metropolitan New Orleans.^- ^

• White females in New Orleans had the lowest in-
cidence rate for cancer of the uterine corpus in the
country — about half the national average.^

• Lung cancer surpassed breast cancer to become the
leading cause of cancer death for Louisiana white
women in 1980, six years prior to the predicted time
for the nation.^

• A marked decrease in mortality for Hodgkin's dis-
ease was observed from 1974 to 1981 while inci-
dence remained stable. This strongly suggests im-
provement in survival resulting from advances in
clinical management — a positive impact on the
health of the Louisiana population.^

• Age-specific mortality for cancers of the oral cavity
and pharynx, esophagus, and larynx exhibited a 2-
slope curve. This apparently indicates either a non-
homogeneous delivery of carcinogens over time or
an increase in incidence in younger cohorts by the
introduction of a new carcinogen or an increase in
the dose of an old one.^

• Pre-menopausal peaks were found in both age-spe-
cific incidence and mortality curves for cervical can-
cer in both white and black Louisiana women, sug-
gesting a new emerging epidemiologic pattern for
this disease.^' ^

• Atypical mortality curves which were observed for
cancers of the ovary, bladder, kidney, and multiple
myeloma need further research.^

CONCLUSIONS

These observations represent only a fraction of the
new information which has become available in Lou-
isiana through the LTR. It is hoped that this wealth
of information will be increasingly utilized by our
health professionals for a better understanding of our
cancer problem and for a concerted effort to meet the
allenge of our considerable cancer burden. The con-
tribution of the LTR to cancer research and control is
a tribute to the Louisiana physicians who have made
it possible. The LTR is a resource for those who are
concerned about cancer in Louisiana. ■

To obtain services or to receive a copy of Cancer in
Louisiana, please write to Jean Craig, Director, Louisiana
Tumor Registry, PO Box 60630, New Orleans, LA 70160.

REFERENCES

1. Correa P, Chen VW, Craig JF, et al: Cancer in Louisiana. Baton Rouge, La,
Louisiana Division of Administration, 1984.

JOURNAL VOL 140 APRIL 53

2. Correa P, Chen VW, Craig JF, et al: Cancer in Louisiana, vol 2. Baton Rouge,
La, Louisiana Division of Administration, 1985.

3. Young JL, Perq^ CL, Asire AT: Surveillance, Epidemiology and End Results:
Incidence and Mortality Data 1973-1977. National Cancer Institute publi-
cation No. 81-2330. Dept of Health and Human Resources, 1981.

4. Waterhouse J, Muir C, Shanmugaratnam K, et al: Cancer Incidence in Five
Continents, vol 4, publication No. 42. Lyon, France, International Agency
for Research on Cancer, 1982, 671-789.

5. Correa P, Chen VW, Craig JF, et al: Cancer in Louisiana, vol 3. Baton Rouge,
La, Louisiana State University Graphic Services, 1986.

6. Chen V, Craig JF, Correa P, et al: Cancer in Louisiana, vol 4. Baton Rouge,
La, Louisiana State University Graphic Services, 1987.

Ms Craig is director of the Louisiana Tumor Registry, Dept of Health
and Human Resources Office of Preventive and Public Health Services

in New Orleans.

Drs Chen, Correa, and Fontham are from the Dept of Pathology at
Louisiana State University Medical Center in New Orleans.

Reprint requests should he sent to Jean F. Craig, Louisiana Tumor
Registry, PO Box 60630, Room 305, New Orleans, LA 70160.

Dx: recurrent

EASI HlOH SI

herpes labialis

“HERPECIN-L is my treatment of choice for
perioral herpes.” GP, NY

”HERPEC1N*L appears to actually prevent the
blisters . . . used soon enough.” DOS, MN

“HERPECIN-L^. . . a conservative approach
with lovir risk/high benefits.” MD, FL

“Used at prodromal symptoms . . . blisters
never formed . . . remarkable.” DH, MA

“(Irt clinical trials) . . . response was dramatic.
HERPECIN-L . .proven far superior.” DOS, PA

“All patients claimed shorter duration ... at
prodromal symptoms . . . HERPECIN L
averted the attacks.” MD, AK

OTC. See P.D.R. for information. For samples to make
your own clinical evaluation, write; Campbell Laboratories,
Inc.. P.O. BOX 812*MD, FDR STATION, NEW YORK, N.Y.
10150

In Louisiana HERPECIN-L is available at all Eckerd,
K & B and Walgreens and other select pharmacies.

LOUISIANA CANCER AND LUNG
TRUST FUND BOARD

ELECK CRAIG, MS; CHARLES L. BROWN JR, MD

The Louisiana Cancer and Lung Trust Fund Board,
which was established in 1980, encourages research
on Louisiana's cancer problem by awarding grants
on topics related to cancer in Louisiana. Support
for the research and for the Louisiana Tumor
Registry, which is supervised by the Louisiana
Cancer and Lung Trust Fund Board, is provided by
funding from a dedicated cigarette tax. Titles of
funded applications are listed along with a brief
description of the Louisiana Cancer Consortium
which was also established through the efforts of
the Louisiana Cancer and Lung Trust Fund Board.

The need for additional funding for cancer
research to combat the serious cancer burden in

Louisiana is emphasized.

T he Louisiana Cancer and Lung Trust Fund Board
was created in 1980 by Legislative Act 825 and was
administratively placed within the Department of
Health and Human Resources. The Board has two
major mandates from the state legislature: to oversee
the Louisiana Tumor Registry, a population-based
registry providing data on the incidence of cancer in
the state; and to encourage, through the awarding of
grants, research on the cancer problem in Louisiana.

FUNDING

Since 1984, the Louisiana Cancer and Lung Trust Fund
Board has received 1 million dollars per year in ded-
icated tobacco taxes. In addition, the Board is au-
thorized to receive contributions for cancer research.

ORGANIZATIONAL STRUCTURE

Officers of the Board include a chairman, vice-chair-
man, and secretary-treasurer. There are four active
committees: Budget, Tumor Registry, Research, and
Advisory. The Board meets a minimum of three times
a year. Members do not receive any compensation for ►

JOURNAL VOL 140 APRIL 55

their services and are entitled only to reimbursement
for travel expenses.

BOARD MEMBERSHIP

The members of the Board representing eleven insti-
tutions are appointed by the governor. Current mem-
bers of the Board and the organizations they represent
are:

Charles L. Brown Jr, MD, chairman, New Orleans
(representing American Cancer Society)

George H. Porter III, MD, vice-chairman, New Orleans
(representing Alton Ochsner Medical Foundation)
Andrew S. Ranier, MD, secretary-treasurer. Lake
Charles

(representing Louisiana State Medical Society)
Lawrence S. Baum, PhD, Monroe
(representing American Lung Association)

R. Davilene Carter, MD, Metairie
(representing Tulane Medical School)

Pelayo Correa, MD, New Orleans
(representing LSU Medical Center-New Orleans)

Carl G. Kardinal, MD, New Orleans
(representing Leukemia Society of Louisiana)

Michael H. Martin, MBA, Baton Rouge
(representing Perkins Radiation Center)

John M. Rainey, MD, Lafayette

(representing Acadiana Medical Research Foundation)
George J. Thomas Jr, MD, New Orleans
(representing Flint-Goodridge Hospital)

Darryl M. Williams, MD, Shreveport
(representing LSU Medical Center-Shreveport)

PROGRESS

The establishment of a statewide tumor registry, as
mandated by the legislature, has been pursued by a
step-wise coverage of the state initiated in the New
Orleans metropolitan area and completed in 1988 with
the coverage of the Alexandria area. A state tumor
registry provides information on incidence, mortality,
and survival of cancer patients. These data are the
basic building blocks for research in cancer epide-
miology and for designing strategies of cancer control
in the state.

The second mandate was to fund research proj-
ects. In the last three years, the Board has funded the
following 22 research projects related to cancer in Lou-
isiana:

Comparison of nutrient, pesticide, and mineral removal in
home tap filters

Detoxification of chemically contaminated drinking water
Screening for carcinogenic exposures in exfoliated human
cells

Conference on the use of aquatic animals as indicators of
environmental pollution

Occurrence of the carcinogen safrole in Louisiana's food
Chromosomal aberrations and neoplastic disposition
Transplacental tobacco exposures
Heredity of lung cancer in Acadians
Cancer rates in Mississippi River catfish: A pilot study
Racial differences in the prognosis of cancer of uterine corpus
Risk factors of cancer of the uterine corpus in New Orleans
The role of genetic predisposition in childhood neoplasia
Worksite smoking control, discouragement, and cessation
Carcinogens in rural groundwater and human blood
Risk assessment for trihalomethanes in northeast Louisiana
Volatile synthetic organics in mother's milk
Lung cancer in non-smoking women, radon exposure
A comparison of treatment strategies for smoking cessation
Pilot of a school-based smoking prevention program for ninth
graders

Immunopathogenesis of bronchogenic carcinoma in Loui-
siana asbestos-exposed population

Summaries of completed research projects funded by
the board are included in Cancer in Louisiana published
annually by the Louisiana Tumor Registry.

In 1985 the Board funded the Louisiana Cancer
Consortium. The aim of the Consortium, as envi-
sioned by the Board, was to bring all academic insti-
tutions into one group to plan and develop cancer
control research activities which would be eligible for
federal funding. The Consortium would in effect be
a cancer research center without walls. Members of
the Consortium include: Louisiana State University
Medical School-New Orleans, Louisiana State Uni-
versity Medical School-Shreveport, Tulane University
School of Medicine, Tulane School of Public Health
and Tropical Medicine, Alton Ochsner Medical Foun-
dation, and the Department of Health and Human
Resources. After three years of funding by the Board,
the future of the Louisiana Cancer Consortium ap-
pears assured as it has been incorporated as a non-
profit organization and the member organizations have
agreed to assume financial responsibility for a full-
time director. The Consortium has begun several col-
laborative pilot projects including a survey of re-

56 JOURNAL VOL 140 APRIL

BOOKS RECEIVED

sources for cancer in Louisiana and has gained sup-
port from major cancer institutions and schools in the
state.

! FUTURE PLANS

The total projected cost of the research applications
received by the Board in the last three years was
$3,298,222, but only $577,045 was available for re-
search. Many peer-approved applications are going
unfunded. The price of scientific research is high, but
it must be continued. Even though Louisiana has a
high cancer rate, it does not receive its share of federal
resources to investigate or combat the problem. By
awarding seed money to investigators for research,
Louisiana will attract both scientists and federal fund-
I ing for future research.

I Now that the Board has completed the tumor
registry expansion, cancer statistics will be available
to be used for cancer research activities statewide.
Using the information gathered, analytic studies are
I being planned to address the cancer problem in Lou-
isiana. New operating funds will be required to im-
plement a new data storage system. This system is
necessary to allow us to interact with similar computer
systems throughout the United States.

An effort will be made to continue acquiring mon-
ies, from private and governmental sources, for the
Board's many activities. The monies available need to
be increased by at least 100% in order to fully carry
out the mission of the Board. ■

For additional information, please contact Dr Charles
L. Brown Jr, Chairman, 200 West Esplanade, Kenner, LA
70065, (504) 464-8600 or Mr Eleck Craig, Administrator,
PO Box 60630, New Orleans, LA 70160, (504) 568-2606.

Mr Craig is administrator of the Louisiana Cancer and Lung Trust
Fund, Louisiana Department of Health and Human Resources, Office of
Preventive and Public Health Services in New Orleans.

Dr Brown is chairman of the Louisiana Cancer and Lung Trust Fund
Board. He is also a clinical professor of medicine at Tulane University
and is in private practice at the Mahorner Clinic in New Orleans.

Reprint requests should be sent to Eleck Craig, Louisiana Cancer and

Lung Trust Fund, PO Box 60630,
New Orleans, LA 70160.

The JOURNAL seeks reviews of the following books. Interested
physicians should contact Frank J. Ilardi, MD, Book Review Editor,
5000 Highway 190, Suite D-3, Covington, LA 70433.

PRACTICAL MICROSCOPIC HEMATOLOGY:

A MANUAL FOR THE CLINICAL LABORATORY
AND CLINICAL PRACTICE

Fritz Heckner, MD, H. Peter Lehmann, PhD, Yuan S. Kao,
MD; Baltimore, Urban & Schwarzenberg Inc, 1988, 97 pages.

CLINICAL ELECTROCARDIOGRAPHY:

A PRIMARY CARE APPROACH

Ken Grauer, MD, R. Whitney Curry, Jr, MD; Oradell, NJ,
Medical Economics Books, 1987, 544 pages.

OB/GYN EMERGENCIES: THE FIRST SIXTY MINUTES
Roy Farrell, MD (ed); Rockville, MD, Aspen Publishers Inc,

1986, 340 pages.

ENDOCERVICAL CARCINOMA:

A CERVICOSCOPIC ATLAS

Minoru Ueki, MD; St Louis, Ishiyaku Euroamerica Inc, 1987,
90 pages.

THE CLINICAL GENETICS HANDBOOK

Ruth Berini (ed); Oradell, NJ, Medical Economics Books, 1986,
385 pages.

INTERPRETING CARDIAC DYSRHYTHMIAS

Marcus Wharton, MD, Nora Goldschlager, MD; Oradell, NJ,
Medical Economics Books, 1986, 241 pages.

NEUROLOGY: PROBLEMS IN PRIMARY CARE

James L. Bernat, MD, Frederick M. Vincent, MD; Oradell,

NJ, Medical Economics Books, 1987, 656 pages.

INFORMED CONSENT: A SURVIVAL GUIDE

Donald J. Palmisano, MD, JD, Hebert J. Mang Jr, JD; New

Orleans, Invictus Publishing Co, 1987, 47 pages.

TO BE OR NOT TO BE HUMAN:

THE TRAITS OF HUMAN NATURE

Ben Freedman, MD; New York, Vantage Press, 1987, 509
pages.

THE AGE OF MIRACLES

Guy Williams; Chicago, Academy Chicago Publishers, 1987,
221 pages.

PRIMARY CARE OF CANCER

Edward A. Mortimer Jr, MD (ed); Cleveland, Case Western
Reserve University School of Medicine, 1987, 190 pages.

HEALING INTO LIFE AND DEATH

Stephen Levine; Garden City, NY, Anchor Press/Doubleday,

1987, 290 pages.

SICKLE-CELL ANEMIA AND THALASSEMIA

Newfoundland, Canada, Canadian Sickle-Cell Society, 1987.

JOURNAL VOL 140 APRIL 57

PROFESSIONAL LISTINGS

THE FERTILITY INSTITUTE OF NEW ORLEANS

{A Professional Corporation)

Richard P. Dickey, MD, PhD Steven N. Taylor, MD

Diplomate, American Board of Diplomate, American Board of

Reproductive Medicine Obstetrics and Gynecology

Diplomate, American Board of
Obstetrics and Gynecology

David N. Curole, MD Phillip H. Rye, MD Terry Olar, PhD

Diplomate, American Board Diplomate, American Board Director, InVitro Laboratory

of Obstetrics and Gynecology of Obstetrics and Gynecology Member, Society for the

Study of Reproduction

REFERRALS ACCEPTED FOR IN VITRO FERTILIZATION
AND OTHER INFERTILITY THERAPY INCLUDING:

MAIN OFFICE

SLIDELL OFFICE

UPTOWN OFFICE

6020 Bullard Ave
New Orleans, LA 70128
(504) 246-8971
(504) 246-8795

700 Cause Blvd
Suite 101
Slidell, LA 70458

2633 Napoleon Ave
Suite 805

New Orleans, LA 70115

TOURO INFIRMARY'S CENTER FOR CHRONIC PAIN

1401 Foucher St
New Orleans, LA 70115
(504) 897-8404

AND

DISABILITY REHABILITATION

Richard H. Morse, MD

Medical Director

Jackie Chauvet

Liaison Coordinator

Elizabeth Messina, RN

Unit Supervisor

58 JOURNAL VOL 140 APRIL

BwaiaaBrnni a iwi w wafliifli^

stages

kiDrwffy

UNIVERSITY OF MARYLAND
BALTIMORE

JUN 2 1988

stacit^

Mca

MOT 10 CIRC.

JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY May 1988

VJ^

Louisiana

Physicians

Insurance Agency, INC.

A WholK' Owned Subsidiar\' c)t LAMMICO

SPECIALLY PRICED PRODUCTS OFFERED:

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A COMMITMENT TO SERVE THE LOUISIANA PHYSICIAN

EDITOR

CONWAY S. MAGEE, MD

CHIEF EXECUTIVE OFFICER

DAVE TARVER

GENERAL MANAGER

RENE ABADIE

MANAGING EDITOR

BONNIE L. BLUNDELL

ADVERTISING SALES

CHARLOTTE SPOONER

JOURNAL COMMITTEE

Chairman, CONWAY S. MAGEE, MD
A.G. KLEINSCHMIDT JR, MD
PAUL F. LARSON, MD
W. CHARLES MILLER, MD
EMILE K. VENTRE JR, MD
Ex officio, DANIEL H. JOHNSON JR, MD

EDITORIAL BOARD

KENNETH B. FARRIS, MD
RODNEY C. JUNG, MD
CONWAY S. MAGEE, MD
W. CHARLES MILLER, MD
ELI SORROW, MD
CLAY A. WAGGENSPACK JR, MD
WINSTON H. WEESE, MD
PATRICK W. PEAVY, MD

PANEL OF CONSULTANTS

KENNETH T. CALAMIA, MD
DELMAR R. CALDWELL, MD
MICHAEL E. CAREY, MD
JOHN COOKSEY, MD
EUGENE J. DABEZIES, MD
ROBERT S. DANIELS, MD
ADOLPH A. FLORES JR, MD
FRANK J. ILARDI, MD
HENRY W. JOLLY JR, MD
TERRY R. JONES, MD
SHELDON P. KOTTLE, MD
MAXIMO B. LAMARCHE, MD
PAUL B. LANSING, MD
SAMUEL A. LEONARD, MD
BROBSON F. LUTZ JR, MD
JOHN c. McDonald, md
PAUL B. MOORE, MD
CHARLES B. ODOM JR, MD
JOHN M. RAINEY, MD
MARY E. SANDERS, MD
JAMES W. VILDIBILL JR, MD
DAVID J. WERNER, MD

ESTABLISHED 1844. Owned and edited by The
Journal of the Louisiana State Medical Society, Inc,
1700 Josephine St, New Orleans, LA 70113.

SUBSCRIPTION PRICE is $12 per year in
advance, postage paid for the United States; $15
per year for all foreign countries belonging to the
Postal Union; $1.50 per single issue.

ADVERTISING: Contact Charlotte Spooner, 1700
Josephine St, New Orleans, LA 70113;
(504) 561-1033, (800) 462-9508.

POSTMASTER: Send address changes to 1700
Josephine St, New Orleans, LA 70113.

THE JOURNAL (ISSN 0024-6921) is published
monthly at 1700 Josephine St, New Orleans, LA
70113. Second-class postage paid at New Orleans
and additional mailing offices.

ARTICLES AND ADVERTISEMENTS published
in the JOURNAL are for the interests of its readers
and do not represent the official position or
endorsement of The Journal of the Louisiana State
Medical Society, Inc or the Louisiana State Medical
Society. The JOURNAL reserves the right to make
the final decision on all content and
advertisements.

I ou

OF THE LOUISIANA STATE MEDICAL SOCIETY

1988

VOLUME 140 / NUMBER 5 / MAY

ARTICLES

Special issue: Cholesterol and coronary heart disease

C. Pratap Reddy, MD

Cholesterol and coronary
heart disease

James W. Cox Jr, MD
C. Pratap Reddy, MD

Cholesterol and coronary
atherosclerosis

Larry J. Leyster, MD
Bryan Lucenta, MD

Diagnosis and evaluation
of hypercholesterolemia

Alfredo Lopez-S, MD, PhD
Barbara Y. Legardeur, MPH

New guidelines for the
treatment of
hyperlipidemia in adults

Barbara Y. Legardeur, MPH
Alfredo Lopez-S, MD, PhD

Dietary treatment of
elevated serum cholesterol

Steven N. Levine, MD

Pharmacologic treatment of
hypercholesterolemia

DEPARTMENTS

Information for Authors

Auxiliary Report

New Members

Books Received

ECG of the Month

Calendar

Otolaryngology/Head
& Neck Surgery Report

Classified Advertising

Cover illustration by Eugene New, New Orleans.

INFORMATION FOR AUTHORS

The JOURNAL welcomes material for publication if submitted by a
Louisiana physician in accordance with the following guidelines. Ad-
dress all correspondence to the Editor, Journal of the Louisiana State
Medical Society, 1 700 Josephine Street, New Orleans, LA 701 1 3. Con-
tact the managing editor with any questions concerning these guidelines
or for a checklist to assist in manuscript preparation.

TITLE PAGE should carry [1 ] the title of the manuscript, which should
be concise but informative; [2] full name of each author, with highest
academic degree(s), listed in descending order of magnitude of con-
tribution (only the names of those who have contributed materially
to the preparation of the manuscript should be included); [3] a one-
to two-sentence biographical description for each author which should
include specialty, practice location, academic appointments, primary
hospital affiliation, or other credits (a picture, black-and-white head
shot, of each author may also be sent if available); [4] name and ad-
dress of author to whom requests for reprints should be addressed,
or a statement that reprints will not be available.

ABSTRACT should be on the second page and consist of no more than
150 words. It is designed to acquaint the potential reader with the
essence of the text and should be informative rather than descriptive.
(Avoid telling what "will be described" and instead describe it.) The
abstract should be intelligible when divorced from the article, devoid
of undefined abbreviations, and suitable, without rewriting, for
reproduction by abstracting services. The abstract should contain: [1]
a brief statement of the manuscript's purpose; [2] the approach used;
[3] the material studied; [4J the results obtained. Emphasize new and
important aspects of the study or observations.

KEY WJ3RDS should follow the abstract and be identified as such.
Provide three to five key words or short phrases that will assist index-
ers in cross-indexing your article. Use terms from the Medical Sub-
ject Heading list from Index Medicus when possible.

jOURNALS

[1] Author(s): Use the surname followed by initials without punctua-
tion. The names of all authors should be given unless there are more
than three, in which case the names of the first three authors are
used, followed by "et al." [2] Title of article. Capitalize only the first
letter of the first word. [3] Name of journal Followed by no punctua-
tion, underscored, and abbreviated according to Index Medicus. [4J
Year of publication; [5] Volume number: Do not include issue number
or month except in the case of a supplement or when pagination is
not consecutive throughout the volume. [6] Inclusive page numbers.
Do not omit digits.

Example: Bora LI, Dannem FJ, Stanford W, et al: A guideline for blood

use during surgery. Am I Clin Pathol 1979;71:680-692.

BOOKS

[1] Author(s): Use the surname followed by initials without punctua-
tion. The names of all authors should be given unless there are more
than three, in which case the names of the first three authors are used
followed by "et al." [2] Title, Capitalize the first and last word and
each word that is not an article, preposition, or conjunction of less
than four letters. [3] Edition number, [4] Editor's name. [5] Place of
publication, [6] Publisher, [7] Year, [8] Inclusive page numbers. Do
not omit digits.

Example: DeCole EL, Spann E, Hurst RA jr, et al: Bedside Examina-

tion in Cardiovascular Medicine, ed 2, Smith JT (ed). New
York, McCraw Hill Co, 1986, pp 23-37.

ILLUSTRATIONS should be submitted in duplicate in an envelope
(paper clips should not be used on illustrations since the indentation
they make may show on reproduction). Legends should be typed,
double-spaced on a separate sheet of paper. Photographic material
should be high-contrast glossy prints. Patients must be unrecognizable
in photographs unless specific written consent has been obtained, in
which case a copy of the authorization should accompany the
manuscript. Omit illustrations which do not increase understanding
of text. Illustrations must be limited to a reasonable number (four il-
lustrations should be adequate fora manuscript of 4 to 5 typed pages).
The following information should be typed on a label and affixed to
the back of each illustration: figure number, title of manuscript, name
of senior author, and arrow indicating top.

TABLES should be self-explanatory and should supplement, not
duplicate, the text. Each should be typed on a separate sheet of paper,
numbered, and have a brief descriptive title.

GALLEY PROOFS will be mailed to the principal author for correc-
tions. Reprint orders forms will accompany galley proofs.

NEW MEMBERS

Applications for membership have been re-
ceived from the following physicians by the
respective parish medical societies as of
Februarv 4, 1988. The Louisiana State Med-
ical Society is pleased to welcome:

■ Allen

Chemparathy V, Manuel, MD

809 East Seventh Ave, Oakdale 71463
1978, Nalanda Medical College, India
internal medicine

■ Calcasieu

Stephen L. Carter II, MD

2903 First Ave, Lake Charles 70602

1980, LSU School of Medicine, New Orleans

pediatrics

William A. Ross, MD

1801 Oak Park, Lake Charles 70601

1982, University of California College of
Medicine, Irvine

internal medicine

■ Jefferson Davis

Martha S. Edwards, MD

1207 S Lake Arthur Ave, Jennings 70546

1983, LSU School of Medicine, New Orleans
internal medicine

■ Orleans

Janet D. Barnes, MD

4335 Elysian Fields, Suite 203, New Orleans
70122

1978, LSU School of Medicine, New Orleans
pediatrics

Mark G. Ewell, MD

1430 Tulane Ave, Dept of Anesthesiology,
New Orleans 70112

1983, Texas Tech University School of Med-
icine, Lubbock

anesthesiology

Emile J. Labranche III, MD

9930 Lake Forest Blvd, New Orleans 70127

1984, LSU School of Medicine, New Orleans
family practice

Sofjam Lamid, MD

1542 Tulane Ave, New Orleans, LA 70112
1960, Faculty of Medicine University of In-
donesia, Indonesia
physical medicine & rehabilitation

Ira. P. Markowitz, MD

3600 Prytania, Suite 71, New Orleans 70130
1981, Medical College of South Carolina,
Charleston
vascular surgery

Mary Beth Murnane, MD

2030 Whitney, New Orleans 70114

1981, LSU School of Medicine, New Orleans

pediatrics

Glenda J. Richardson, MD

2222 Simon Bolivar, New Orleans 70113

1977, LSU School of Medicine, New Orleans
pediatrics

Ellis E. Williams, MD

4335 Elysian Fields, Suite 303, New Orleans
70122

1978, University of Michigan Medical School,
Ann Arbor

internal medicine

Robert A. Zimmerman, MD

2700 Napoleon Ave, New Orleans 70113
1983, Tulane University School of Medicine,
New Orleans
emergency medicine

■ Rapides

Robin R, Bennett, MD

PO Box 13030, Alexandria 71315

1978, LSU School of Medicine, New Orleans

internal medicine

Wesley W. Davis, MD

405 Third St, Alexandria 71301

1980, LSU School of Medicine, Shreveport

cardiology

James G. Ralston, MD

65 Medical Park Blvd, Suite 101, PineviUe
71360

1982, LSU School of Medicine, Shreveport
ophthalmology

Andrew P. Terry, MD

3311 Prescott Rd, Suite 200, Alexandria 71301

1983, University of Alabama School of Med-
icine, Birmingham

ophthalmology

■ IntemI Resident Members

ORLEANS

James T. LeMay, MD

1542 Tulane Ave, New Orleans 70112
1972, University of Mississippi School of
Medicine, Jackson
psychiatry

JOURNAL VOL 140 MAY 3

E douard C. (Ed) Carrere, Jr.
attended St. Stanislaus
from 1934-1939. He went
on to become a partner in
Ernest A. Carrere s Sons in
New Orleans and has served
on the Board of Directors of the

American Red Cross, the Presidents Council
of Loyola University, and as President of the
Real Estate Commission of New Orleans.
“The virtues of honesty and integrity instilled
in me at St. Stanislaus were the trademark
of my business. My word is my bond”

To the Brothers of the Sacred Heart,
every student is a potential leader. And giving
him the proper example— spiritual, intellectual
and moral — is our mission at St. Stanislaus.

BOARDING SCHOOL GRADES 6-12
SUMMER CAMP AGES 9-14

304 South Beach Blvd. Bay St. Louis, MS 39520

SAIIMT STy\IMISI-ALJS

St Stanislaiis
helps build leaders.

FOR A FREE BROCHURE CALL THE DIRECTOR OF ADMISSI0NS-(601) 467-9057.

Norton W. Voorhies, MD, Editor

ECG OF THE MONTH

MORE THAN MEETS THE EYE

JORGE I. MARTINEZ-LOPEZ, MD

The continuous rhythm strip shown below, limb lead II, was recorded on a 58-year-old man with severe
chronic obstructive lung disease.

What is your diagnosis? Elucidation is on page 7.

JOURNAL VOL 140 MAY 5

Now America’s
oldest professional

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ECG Of the Month

Case presentation is on page 5.

DIAGNOSIS — Sinus rhythm; atrial parasystole

The most obvious finding in the tracing (courtesy of
Dr. William P. Nelson) is the presence of P waves
with two different morphologies: one is broad and
notched; the other is tall and peaked. The broad and
notched P waves are of sinus node origin, recur at a
rate of 65 times a minute, and are associated with
normal PR, QRS, and QT intervals, and normal ST
segments and T waves.

The tall, peaked P waves, on the other hand, are
ectopic and their positive polarity indicates a high
right atrial origin. Ectopic P waves appear frequently
during the recording — mostly in a trigeminal pattern
— at rates slower than the sinus rhythm, and are
followed by QRS complexes that are either similar to
or broader and different in configuration than those
of the sinus rhythm, and by normal ST segments and
T waves.

It is the nature of these ectopic P waves (EP) that
forms the basis for the discussion to follow.

DISCUSSION

It would be very easy to summarily dismiss the ar-
rhythmia shown in the tracing as the result of atrial
premature impulses. However, careful analysis of the
rhythm strip reveals more than meets the eye.

Atrial premature impulses usually display fixed
coupling intervals because they are dependent on the
preceding cycle. In contrast, the coupling intervals
between EPs and sinus Ps in the tracing are variable:
some EPs occur late in diastole, while others occur in
early or mid-diastole. Even though the coupling in-
tervals are variable, intervals between consecutive EPs
(interectopic intervals) are relatively constant except
in the middle panel, where the first EP-to-EP interval
is longer than the preceding and the following inter-
ectopic intervals. Lastly, all but two of the EP-to-sinus
P intervals (the returning cycles) are longer than the
sinus cycles; the two that are not are about equal to
the sinus cycles.

The combination of EPs associated with variable
coupling intervals and with interectopic intervals that
are either equal to or close multiples of a common
denominator should prompt the interpreter to con-

sider the ECG diagnosis of atrial parasystole.

At this time, it is important to present briefly the
concept of parasystole. Normally, depolarization of
the heart is initiated and dominated by impulses gen-
erated by the sinus node. Dual cardiac rhythms can
occur when two separate pacemakers are concur-
rently in operation, eg, complete AV block and other
forms of AV dissociation and parasystole.

The term parasystole (from the Greek, beating side-
by-side) designates a group of arrhythmias in which
there is "dual activation of a single cardiac chamber
in which one pacemaker (the parasysfoHc one) is pro-
tected intermittently or totally from discharge by the
prevailing rhythm." The parasystolic focus (PF) has
special characteristics. First, it is ectopic and may be
located an 5 nvhere in the heart. Most commonly, PF
is located in the ventricles, less commonly in the AV
node, and rarely in the atria; other reported sites in-
clude the bundle of His and accessory cardiac path-
ways. Second, PF is an independent automatic center
of impulse formation with two other characteristics:
entrance and exit block. Entrance block protects PF from
extinction by advancing electrical fronts that other-
wise would invade its domain, discharging and sup-
pressing it. As a result, PF can fire regularly, undis-
turbed by other electrical impulses. Exit block, on the
other hand, occurs in the opposite direction of en-
trance block and confines the ectopic impulse to PF.
The degree of exit block exhibited by PF will deter-
mine the observed manifest rate.

The exact location of PF in atrial parasystole is
not known; a location within a major atrial prefer-
ential conduction pathway in the right atrium has
been proposed. When an atrial PF and sinus rhythm
coexist, both compete to activate the atria and ven-
tricles; the focus with the faster rate of firing will be
the dominant pacemaker of the heart. Manifest rates
of between 20 and 375 a minute have been reported
in atrial parasystole, but rates of 40 or less are more
common.

Although atrial parasystole is not abolished by
sinus impulses, maneuvers that transiently increase
vagal tone, as well as mild exercise or isoproterenol,
may terminate atrial parasystole. Conversely, the sinus
node is not protected from atrial parasystolic impulses
and may be discharged and reset by them. A variety
of factors determine whether or not the sinus node
will be discharged and reset by atrial parasystolic im-
pulses.

JOURNAL VOL 140 MAY 7

The variation in the morphology of the QRS com-
plexes that follow EPs in the tracing is attributed to
the degree of refractoriness encountered downgrade
by the advancing ectopic electrical impulses: narrow
QRS complexes denote normal, and wide QRS com-
plexes aberrant, ventricular conduction.

In general, treatment of atrial parasystole is not
required because the arrhythmia is benign and usu-
ally produces neither cardiac symptoms nor hemo-
dynamic changes. In most instances, reassurance of
the patient, the use of sedatives — if the patient is
apprehensive — and management of the underlying
cardiac disease is all that is necessary. The patient
whose tracing is shown here had repetitive episodes
of atrial parasystole for at least three years, but at no
time did he have episodes of triggered atrial activity.
Once during the three-year period, oral quinidine was
given; it failed to suppress the arrhythmia, but pro-
voked a devastating diarrhea.

Atrial parasystole goes unrecognized frequently
because it is a rare cardiac arrhythmia and because
many physicians are not familiar with it and will er-
roneously identify the ectopic P waves as atrial pre-
mature impulses. Because the 12-lead ECG is not of
sufficient length to raise the index of suspicion, a long
rhythm strip is desirable and will show more than
meets the eye. ■

SELECTED REFERENCES

1. Langendorf R, Lesser ME, Plotkin P, et al: Atrial parasystole with inter-
polation. Am Heart J 1962;63:649-658.

2. Flowers NC, Copeland GD, Brody DA: Two cases of supraventricular
parasystole. Circulation 1964;29:440-446.

3. Eliakim M: Atrial parasystole: Effects of carotid sinus stimulation, Valsalva
maneuver and exercise. Am J Cardiol 1965;16:457-461.

4. Friedberg HD, Schamroth L: Atrial parasystole. Br Heart J 1970;32:172-
180.

5. Pick A, Langendorf R: Parasystole and its variants. Med Clin North Am
1976;60:125-147.

Dr. Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to he construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

ARAFATE"

^(sucralfate) Tablets

BRIEF SUMMARY

CONTRAINDICATIONS

There are no known contraindications to the use of sucralfate.

PRECAUTIONS

Duodenal ulcer is a chronic, recurrent disease. While short-term treatment with sucralfate
can result in complete healing of the ulcer, a successful course of treatment with
sucralfate should not be expected to alter the post-healing frequency or severity of
duodenal ulceration.

Drug Interactions: Animal studies have shown that simultaneous administration
of CARAFATE (sucralfate) with tetracycline, phenytoin, digoxin, or cimetidine will result
in a statistically significant reduction in the bioavailability of these agents. The bioavailability
of these agents may be restored simply by separating the administration of these
agents from that of CARAFATE by two hours. This interaction appears to be nonsys-
temic in origin, presumably resulting from these agents being bound by CARAFATE in
the gastrointestinal tract. The clinical significance of these animal studies is yet to be
defined. Howevei; because of the potential of CARAFATE to alter the absorption of
some drugs from the gastrointestinal tract, the separate administration of CARAFATE
from that of other agents should be considered when alterations in bioavailability are felt
to be critical for concomitantly administered drugs.

Carcinogenesis, Mutagenesis, Impairment of Fertility: Chronic oral toxicity
studies of 24 months' duration were conducted in mice and rats at doses up to 1 gm/kg
(12 times the human dose). There was no evidence of drug-related tumorigenicity. A
reproduction study in rats at doses up to 38 times the human dose did not reveal any
indication of fertility impairment. Mutagenicity studies were not conducted.

Pregnancy: Teratogenic effects. Pregnancy Category B. Teratogenicity studies
have been performed in mice, rats, and rabbits at doses up to 50 times the human dose
and have revealed no evidence of harm to the fetus due to sucralfate. There are,
however, no adequate and well-controlled studies in pregnant women. Because animal
reproduction studies are not always predictive of human response, this drug should be
used during pregnancy only if clearly needed.

Nursing Mothers: It is not known whether this drug is excreted in human milk.
Because many drugs are excreted in human milk, caution should be exercised when
sucralfate is administered to a nursing woman.

Pediatric Use: Safety and effectiveness in children have not been established.

ADVERSE REACTIONS

Adverse reactions to sucralfate in clinical trials were minor and only rarely led to
discontinuation of the drug. In studies involving over 2,500 patients treated with sucralfate,
adverse effects were reported in 121 (4.7%).

Constipation was the most frequent complaint (2.2%). Other adverse effects, reported
ih no more than one of every 350 patients, were diarrhea, nausea, gastric discomfort,
indigestion, dry mouth, rash, pruritus, back pain, dizziness, sleepiness, and vertigo.

OVERDOSAGE

There is no experience in humans with overdosage. Acute oral toxicity studies in
animals, however using doses up to 1 2 gm/kg body weight, could not find a lethal dose.
Risks associated with overdosage should, therefore, be minimal.

DOSAGE AND ADMINISTRATION

The recommended adult oral dosage for duodenal ulcer is 1 gm four times a day on
an empty stomach.

Antacids may be prescribed as needed for relief of pain but should not be taken
within one-half hour before or after sucralfate.

While healing with sucralfate may occur during the first week or two, treatment
should be continued for 4 to 8 weeks unless healing has been demonstrated by x-ray or
endoscopic examination.

HOW SUPPLIED

CARAFATE (sucralfate) 1-gm tablets are supplied in bottles of 100 (NDC 0088-1712-47)
and in Unit Dose Identification Paks of 100 (NDC 0088-1712-49). Light pink scored
oblong tablets are embossed with CARAFATE on one side and 1712 bracketed by Cs on
the other. Issued 1/87

References:

1. Korman MG, Shaw RG, Hansky J, etal: Gasfroenfero/ogy 80:1451-1453, 1981.

2. Korman MG, Hansky J, Merrett AC, etal: D;g D/s Sc/ 27:71 2-71 5, 1982.

3. Brandstaetter G, Kratochvil P: Am J Med 79 (suppi 2C):36-38, 1985.

4. Marks IN, Wright JR Gilinsky NH, et al: J Clin Gastroenterol 8:419-423, 1986.

5. Lam SK, Hui WM, Lau WY, etal: Gasfroenfero/ogy 92:1193-1201, 1987.

Another patient benefit product from

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8 JOURNAL VOL 140 MAY

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

EVALUATION OF FACIAL NERVE

PARALYSIS

J. KEVIN DUPLECHAIN, MD; PAUL A. BLAIR, MD, FACS

Evaluation of facial paralysis is a difficult
problem. We present a brief case presentation of a
patient who developed facial paralysis secondary
to a blow on the head. His workup and eventual
outcome is detailed. This allows for a broad
review of different causes of facial nerve paralysis,
and in detail, describes current diagnostic studies
that help in determining these causes and eventual

outcome.

A 37-year-old black male came to the otolaryngol-
ogy clinic four days after being struck on the left
side of the head complaining of left-sided facial pa-
ralysis. On the day the injury occurred, he was taken
to the emergency room for evaluation because he was
momentarily unconscious. Physical examination, plain
skull films, and computed tomography scan of the
head were normal. At presentation to our cUnic com-
plete left-sided facial paralysis was evident. The re-
mainder of his examination was significant only for
a left middle ear effusion. Computed tomography
scans were reviewed without evidence of a fracture.
Nerve excitability testing (NET) using the Hilger stim-
ulator revealed no asymmetry. Audiogram demon-
strated a mild conductive loss in the left ear and an
absent stapedius reflex. He was admitted to the hos-
pital, placed on intravenous steroids, and underwent
serial nerve excitability testing. On the fourth hospital
day, a 1.5 milliamp difference was noted during NET.
Intravenous steroids were continued, and two days
later facial function began to return. He was subse-
quently discharged and follow-up evaluation revealed
approximately 90% return of facial nerve function.

JOURNAL VOL 140 MAY 11

DISCUSSION

Facial nerve paralysis can be a distressing condition
for both patient and physician. Whether the etiology
is traumatic, neoplastic, or idiopathic, careful evalu-
ation of nerve function is essential. Historical points
in the evaluation include a history of trauma to the
head and/or face, previous episodes of facial paralysis
and rapidity of onset of the paralysis. In the trau-
matized patient, acute onset of paralysis may indicate
complete transection of the nerve, in which case ex-
ploration should be undertaken. A slow and pro-
gressive palsy over several days suggests a stretch
type injury. Delayed onset of paralysis, usually greater
than three weeks, is most suspicious for a neoplastic
process. Idiopathic facial paralysis (ie, BelFs palsy)
may present with a complete and sudden onset of
paralysis or a slower progressive palsy, with prog-
nosis for recovery worse in the former.

Recurrent facial paralysis can be grouped into
ipsHateral, alternating, and bilateral. Ipsilateral con-
ditions are associated with neoplastic processes.
Schwannomas have been the most common benign
neoplasm causing unilateral facial paralysis.^ Schwan-
nomas arise with equal incidence from the facial and
acoustic nerves. Alternating recurrent facial paralysis
occurs approximately 12% of the time in Bell's palsy.
Of the more unusual conditions that cause alternating
facial paralysis, Melkerson Rosenthal Syndrome (MRS)
is the most common. Other characteristics of MRS
include recurrent edema of the lips, face and eyelids,
cheilitis, and a fissured tongue.

Bilateral simultaneous paralysis can be a result of
neurologic disease such as Guillian Barre Syndrome,
granulomatous diseases including sarcoidosis, or other
neoplastic disorders such as leukemia.

ANATOMY OF THE FACIAL NERVE

The facial nerve (Fig) originates from the pons and
emerges from the brainstem with the nervous inter-
medius, and then joins the acoustic nerve to enter
into the internal auditory canal. Distal to this point,
the nerve enters the fallopian canal which can be di-
vided into 3 segments: 1) labyrinthine segment, 2)
tympanic or horizontal segment, and 3) mastoid or
vertical segment. The labyrinthine segment of the fal-
lopian canal extends from the fundus of the internal

Fig. Anatomy of the facial nerve through the tem-
poral bone

auditory canal to just distal to the geniculate ganglion.
The nerve is exquisitely sensitive to injury here be-
cause the canal is very narrow, and this segment of
the nerve lacks anastomosing arterial arcades.^

Three nerves originate within this segment. The
greater petrosal nerve sends preganglionic parasym-
pathetic fibers via the pteryogopalatine ganglion to
supply secretory function to the lacrimal gland. An
inconsistent external petrosal nerve carries sympa-
thetic fibers to the middle meningeal artery. The third
branch is the lesser petrosal nerve which supplies
secretomotor function to the parotid gland.

The facial nerve then makes an abrupt turn (genu)
within the temporal bone where the tympanic or hor-
izontal position begins. Within this segment, no
branches arise. The final segment of the nerve within
the fallopian canal gives rise to two separate branches
which subsequently innervate the stapedius muscle
and supply taste to the anterior two-thirds of the
tongue. A thorough understanding of facial nerve
anatomy within the temporal bone is essential for
electrodiagnostic, topognostic studies, audiometric
and radiologic evaluation.

TOPOGNOSTIC TEST

Topognostic tests are site of lesion test. Their utili-
zation is based on the various branches of the facial

12 JOURNAL VOL 140 MAY

nerve within the temporal bone. These tests include
the Schirmer test, submandibular salivary flow test,
stapedius reflex, and electrogustometry. These tests
are commonly utilized in the patient with head trauma
resulting in facial paralysis.

The Schirmer test is a means of quantitating lac-
rimation. Normal results suggest an intact greater pe-
trosal nerve which supplies the lacrimal gland. The
test is performed by placing 5 mm precut portions of
filter paper into the medial third of the lower lid. At
three minutes the test is terminated and a measure
of tear flow is obtained. By comparing the ratio of the
normal to the abnormal side, the likelihood of a nerve
injury in the labyrinthine segment of the facial nerve
can be predicted.^

Submandibular salivary flow is dependent on the
integrity of the chordae tympani which arises within
mastoid segment of the fallopian canal, synapses in
the submandibular ganglion and then innervates the
submandibular gland. Testing consists of selectively
cannulating the ducts in the floor of the mouth, and
the measuring salivary flow for a specified time pe-
riod. Results are abnormal when salivary flow on the
affected side is 25% of the normal side.^

Stapedius reflex evaluation is essential to any
workup in a patient with facial paralysis. Its absence
indicates loss of innervation of the stapedius muscle,
whose nerve supply arises from the mastoid segment
of the facial nerve. Middle ear pathology must be
excluded if this test is to be valid. Electrogustometry
is a means of stimulating the taste receptors within
the tongue electrically to evaluate chordae tympani
integrity.^ The reliability of this test is not good be-
cause of the subjective interpretation of taste by dif-
ferent individuals.

ELECTRODIAGNOSTIC STUDIES

Electroneurography, the general term for diagnostic
studies of nerve dysfunction, has modernized facial
nerve testing. It has become helpful in defining in-
dications for surgical exploration of the temporal bone
in trauma cases, as well as predicting outcome of non-
surgically treated patients with facial nerve dysfunc-
tion.

Different degrees of nerve injury can occur. Tem-
poral bone fractures sometimes result in complete
transection of the nerve, whereas in idiopathic facial
paralysis, edema of the nerve is thought to be the
likely mechanism causing paralysis. Electroneurog-
raphy can help distinguish the varying types of in-

TABLE

SUNDERLAND CLASSIFICATION OF NERVE INJURIES

Class 1

Neuropraxic

No loss of Axonal Continuity
NET symmetric

Class II

Axontemetic

Axonal disruption and Wallerian
degeneration occur
NET asymmetric

Class III

Neurotemetic

Endoneurial disruption occurs

Class IV

Neurotemetic

Perineural disruption occurs

Class V

Neurotemetic

Epineural disruption occurs

Note: Class III, IV, V injuries allow for partial recovery and
synkenisia.

juries. Sunderland classified nerve injuries into five
distinct categories (Table). ^

NET is the most basic of electroneurography. It
is a minimal stimulation test commonly performed
with a Hilger nerve stimulator. It determines minimal
nerve excitatory thresholds and can distinguish neu-
ropraxic from more severe lesions. Testing is per-
formed by comparing the normal to the abnormal side
by stimulating the nerve at its trunk where it exits the
stylomastoid foramen. A difference of 3.5 milliamps
between normal and abnormal sides signifies pro-
gressive degeneration of the nerve and significant in-
jury.

Electroneurography is a more standardized and
objective test. It is classified as a maximal or supra-
maximal stimulation test because the voltage is in-
creased on the voltage stimulator until maximal facial
motion is obtained. A recorder electrode is placed on
the nasolabial fold and records muscle twitches caused
by the electrical current. Multiple stimulations are
performed, and an average amplitude is obtained.
This is then compared to the normal amplitudes ob-
tained on the nonparalyzed side. The percentage of
the nerve that has undergone degeneration is calcu-
lated, and 90% degeneration implies that without in-
tervention surgically, the prognosis is poor for recov-
ery.^

Electromyography or the recording of muscle po-
tentials within the facial musculature becomes im-
portant when visible or electrical stimulation cannot ^

JOURNAL VOL 140 MAY 13

be recorded by electroneurography. Characteristic re-
sponses can help predict outcome. In a delayed eval-
uation, approximately four to six weeks post paral-
ysis, electromyography may demonstrate polyphasic
reinnervation potentials indicating nerve regenera-
tion and no reason to alter treatment. However, as
early as 14 days post onset of paralysis, fibrillation
potentials may be present indicating early nerve de-
generation.

AUDIOLOGIC AND RADIOGRAPHIC
EVALUATION

Audiologic evaluation of any patient with facial nerve
paralysis should include pure tone audiogram and
stapedius reflex. In unknown cases of facial paralysis
this can help distinguish neoplastic from idiopathic
causes. In the trauma patient, absence of a stapedius
reflex with an otherwise normal middle ear, indicates
a lesion in the temporal bone. This is especially im-
portant in the trauma patient.

Radiographic evaluation is probably best per-
formed utilizing high resolution computed tomogra-
phy with maximal bone enhancement. Scans should
range from the stylomastoid foramen to the petrous
apex. Axial and coronal views should be obtained.
Pleuridirectional tomograms are also very useful, but
used less. Lateral, anteroposterior, and 20° oblique
views should be obtained, along with internal audi-
tory canal views, a common site for neoplastic proc-
esses.

CONCLUSION

The patient presented sustained a neuropraxic injury
to the facial nerve within the temporal bone. This case
demonstrates the most basic evaluation of a patient

with facial nerve dysfunction. A key point in his his-
tory was that the palsy occurred four days post trauma,
significantly limiting the types of injury that could
have occurred. If the trauma had transected the nerve,
paralysis should have been immediate. Other key
points such as symmetric NET initially, and then a
difference of only 1.5 milliamps subsequently indi-
cates a Class I or II injury. Had NET been greater than
3.5 milliamps, electroneuronography would have been
indicated.

In cases which are not as clearly defined, the
entire battery of topognostic and electrodiagnostic
studies are essential. Again, they can help predict site
of lesion, type of injury, indications for temporal bone
exploration, and prognosis for recovery which are all
essential for appropriate care of patients with facial
nerve paralysis. ■

REFERENCES

1. May M: The Facial Nerve. New York, Thieme Inc, 1986.

2. May M: Total facial nerve exploration. Laryngoscope 1979;89:906.

3. Yagi N: Comparison of thread test of lacrimation to Schirmer test. Ann
Otol Rhinol Laryngol 1986;122:3.

4. May M, Harvey JE: Salivary flow; A prognostic test for facial paralysis.
Laryngoscope 1971;81(2):179.

5. Alford BR: Electrodiagnostic studies in facial paralysis. Arch Otolaryngol
1967;85:259.

6. Dobie R: Electrical and topognoshc test of the facial nerve, in Otolaryn-
gology — Head and Neck Surgery, Cummigs C (ed). St Louis, CV Mosby
Company, 1986.

7. Fisch U; Prognostic value of electrical test in acute facial paralysis. Am }
Otology 1986;5:494.

Dr Duplechain is a resident in the Dept of Otolaryngology — Head and
Neck Surgery at Tulane University Medical Center in

New Orleans.

Dr Blair is a professor of Otolaryngology — Head and Neck Surgery at
Tulane University Medical Center in New Orleans.

Reprints will not be available.

14 JOURNAL VOL 140 MAY

Jackie Tucker, LSMSA President

AUXILIARY REPORT

MEETING THE CHALLENGES OF
TODAY FOR TOMORROW

JACKIE C. TUCKER

I N Shel Silverstein's
book of poems, A
Light in the Attic, there is
a poem entitled “Ham-
mock."

Grandma sent the
hammock

The good Lord sent
the breeze.

Tm here to do the
swinging.

Now who's gonna
move the trees?

There are times I feel this little verse could have been
subtitled "Medicine Today." We need to determine
"who's gonna move the trees." It is time that we
become more responsible for meeting the challenges
that medicine offers today.

A commitment to membership will be one of the
major challenges our auxiliary will undertake this year.
It is imperative that we communicate the importance
of "belonging" and "involvement" to every potential
auxilian in Louisiana. This past year we have formed

two new auxiliaries, Morehouse and Natchitoches,
with fantastic leaders like Carol Chorette, Melissa
Smith, and Cindy Barnum. And as recently as this
past month. Baton Rouge increased its membership
by 116 new members!

Success in our legislature is another challenge to
which we must make a major commitment. We need
more people like Helen Olivier, Ann Reilly Jones, and
Jeanne Buffet to vow to work with our legislators to
assert our positions. To implement this, we are plan-
ning a statewide "Day at the Legislature" where we
can all convene together as an impressive body to
contact our area representatives. We are challenged
to be better communicators. We need to know more
about each other, and more about our neighboring
auxiliary projects. Patti Brannan of Shreveport will be
working toward this goal with a new format for our
Capsulettes.

Already we have begun to meet the challenge of
health and community involvement. Our members
have made such positive impacts across our state —
Terry Anseman of Lafayette, and Ellouise Sneed of
West St Tammany are just two examples. These ladies
have led the way in presenting outstanding, vital ►

JOURNAL VOL 140 MAY

BOOKS RECEIVED

health-related programs to our communities.

We must also maintain the challenge of working
not only in our local auxiliaries, but in understanding
the importance of being active in our state and na-
tional counterparts. It will be through the united ef-
forts of all of us — whether we're from Rapides, North
Central, Orleans, Calcasieu or St Landry — the com-
mitments of auxilians from Bossier to Hammond, from
Terrebonne to Ouachita, and all points in between.
It will take the continuing interest and caring of past
and present board members, and the shared enthu-
siasm of our spouses that will assure us of meeting
these goals.

Our relationships with each other, with other
auxiliaries, and especially with our Louisiana State
Medical Society, are all key to meeting these chal-
lenges fully prepared. A team approach is necessary
in all our plans — our support system must be "built-
in." It's our chance to meet these challenges, and as
the poet wrote, "to move the trees."

Focusing on these challenges is a priority for me
this year. Working together with people like each of
you will assure our success! ■

Mrs Tucker (wife of Dr Robert A. Tucker) is president of the Louisiana

State Medical Society Auxiliary

The JOURNAL seeks reviews of the following books. Interested
physicians should contact Frank J. Ilardi, MD, Book Review Editor,
5000 Highway 190, Suite D-3, Covington, LA 70433.

PRACTICAL MICROSCOPIC HEMATOLOGY:

A MANUAL FOR THE CLINICAL LABORATORY
AND CLINICAL PRACTICE

Fritz Heckner, MD, H. Peter Lehmann, PhD, Yuan S. Kao,
MD; Baltimore, Urban & Schwarzenberg Inc, 1988, 97 pages.

CLINICAL ELECTROCARDIOGRAPHY:

A PRIMARY CARE APPROACH

Ken Grauer, MD, R. Whitney Curry, Jr, MD; Oradell, NJ,
Medical Economics Books, 1987, 544 pages.

OB/GYN EMERGENCIES: THE FIRST SIXTY MINUTES
Roy Farrell, MD (ed); Rockville, MD, Aspen Publishers Inc,

1986, 340 pages.

ENDOCERVICAL CARCINOMA:

A CERVICOSCOPIC ATLAS

Minoru Ueki, MD; St Louis, Ishiyaku Euroamerica Inc, 1987,
90 pages.

THE CLINICAL GENETICS HANDBOOK

Ruth Berini (ed); Oradell, N], Medical Economics Books, 1986,
385 pages.

INTERPRETING CARDIAC DYSRHYTHMIAS

Marcus Wharton, MD, Nora Goldschlager, MD; Oradell, NJ,
Medical Economics Books, 1986, 241 pages.

NEUROLOGY: PROBLEMS IN PRIMARY CARE

James L. Bernat, MD, Frederick M. Vincent, MD; Oradell,

NJ, Medical Economics Books, 1987, 656 pages.

INFORMED CONSENT: A SURVIVAL GUIDE

Donald J. Palmisano, MD, JD, Hebert J. Mang Jr, JD; New

Orleans, Invictus Publishing Co, 1987, 47 pages.

TO BE OR NOT TO BE HUMAN:

THE TRAITS OF HUMAN NATURE

Ben Freedman, MD; New York, Vantage Press, 1987, 509

pages.

THE AGE OF MIRACLES

Guy Williams; Chicago, Academy Chicago Publishers, 1987,
221 pages.

PRIMARY CARE OF CANCER

Edward A. Mortimer Jr, MD (ed); Cleveland, Case Western
Reserve University School of Medicine, 1987, 190 pages.

HEALING INTO LIFE AND DEATH

Stephen Levine; Garden City, NY, Anchor Press/Doubleday,

1987, 290 pages.

SICKLE-CELL ANEMIA AND THALASSEMIA

Newfoundland, Canada, Canadian Sickle-Cell Society, 1987.

JOURNAL VOL 140 MAY

CALENDAR

June

June 1-4

9th Conference on Computer Applications in Radiology,

Hilton Head Island, South Carolina. Contact: Ms. Janice Ford,
Continuing Education Coordinator, Dept of Radiology, Hospital
of the University of Pennsylvania, 3400 Spruce St, Philadelphia,
PA 19104; (215)662-6904, (215)662-6982.

June 6

Annual Instructional Course on the Clinical Application of
Hyperbaric Oxygen, New Orleans. Contact: Jane Dunne,
Undersea & Hyperbaric Medical Society, 9650 Rockville Pike,
Bethesda, MD 20814.

June 9-12

17th Aimual Scientific Assembly of the American College
of Emergency Physicians State Chapter of California Inc,

Rancho Mirage, California. Contact: CAL/ACEP, 505 N
Supulveda Blvd, #12-14, Manhattan Beach, CA 90266;
(213)374-4039.

June 11-12

Workshop on Anesthesia and Vital Organ Fimction, Boston.
Contact: American Society of Anesthesiologists, 515 Busse Hwy,
Park Ridge, U 60068.

June 11-14

Dermatology for Non-Dermatologists, Myrtle Beach, South
Carolina. Contact: Division of Dermatology, Box 3135, Duke
University Medical Center, Durham, NC 27710; (919)684-2504.

June 16-18

33rd Annual Great Smokey Mountain Pediatric Seminar,

Park Vista Hotel, Gatlinburg, Tennessee. Contact: Dr. San-
dra Loucks, University of Tennessee Medical Center, Dept of
Pediatrics, 1924 Alcoa Hwy, Knoxville, TX 37920; (615)544-9331.

June 16-18

AIDS and Infectious Disease Update, Hilton Resort, South
Padre Island, Texas. Contact: Scott and White Office of Con-
tinuing Medical Education, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

June 20-23

1st International Symposium on Orbital Plastic Surgery, San

Francisco. Contact: Plastic Surgery Educational Foundation, 233
N Michigan Ave, Suite 1900, Chicago, 11 60601; (312)228-9900.

June 27-29

Perioperative Red Cell Transfusion, Bethesda, Maryland.

Contact: National Institutes of Health, 9000 Rockmlle Pike,
Bethesda, MD 20852; (301)496-2520.

July

July 1-5

2nd Annual Family Practice Board Review, San Diego. Con-
tact: Office of Continuing Medical Education, UC San Diego School
of Medicine, M-017, La Jolla, CA 92093; (619)534-3940.

July 6-13

Breast Imaging and Ultrasound, Alaska 88: Cruise the In-
land Passage. Contact: Medical Seminars International Inc, 21915
Roscoe Blvd, Suite 222, Canoga Park, CA 91304; (818)719-7380.

July 14-16

4th Annual Berkshire Medical Conference: Advances in Car-
diology, Hancock, Massachusetts. Contact: Berkshire AHEC,
(413)447-2417.

July 17-22

July 19-23

Louisiana Academy of Family Physicians Annual Scientific
Assembly, Sandestin Beach Hilton, Destin, Horida. Contact:
LAPP, 4705 Iberville St, New Orleans, LA 70119.

July 21 - August 2

Italy and the Swiss Alps, Sponsored by INTRAV and the
Louisiana State Medical Society. Contact: Anita Bums, LSMS,
1700 Josephine St, New Orleans, LA 70113; (504)561-1033,
(800)462-9508.

July 24-28

34th Armual Southern OB-GYN Seminar, Asheville, North
Carolina. Contact: Dr. George Schneider, Ochsner Clinic, Dept
of OB-GYN, 1514 Jefferson Hwy, New Orleans, LA 70121;
(504)838-4031.

July 24-29

8th Annual Internal Medicine Review, Hilton Resort, South
Padre Island, Texas. Contact: Scott & White (Continuing Medical
Education Office, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

JOURNAL VOL 140 MAY 19

I N OCTOBER 1987, the National
Heart, Lung and Blood Insti-
tute (NHLBI), in cooperation with
the American Heart Association
and other organizations, launched
a national campaign called the Na-
tional Cholesterol Education Pro-
gram (NCEP). This effort was in-
itiated as a direct result of the
recommendations of the NHLBI
Consensus Conference on Lower-
ing Cholesterol. The Consensus
Conference, after careful considera-
tion of all lines of evidence support-
ing an association between elevated serum cholesterol
and coronary heart disease (CHD), concluded that
there was a cause-and-effect relationship between
serum cholesterol and CHD and that a decline in CHD
mortality in the United States can be affected by con-
trol of hypercholesterolemia. The goal of the NCEP is
to help prevent Ulness and premature death from CHD
by reducing the number of Americans with high serum
cholesterol. The purpose of the NCEP, in the words
of James I. Cleeman, MD, NHLBI program coor-
dinator, "is to educate both professionals and the
public to make it clear how important it is to lower high
cholesterol levels and to explain how to go about it."

Each year, the JOURNAL works with the Physician
Education Committee of the Louisiana Heart Associa-
tion to produce a special issue devoted to car-
diovascular disease. This year, quite appropriately, the
topic for this special issue is the evaluation and
management of hypercholesterolemia. The Physician
Education Committee of the Louisiana Heart Associa-
tion hopes that this issue will provide Louisiana physi-
cians with a strong impetus for implementing the
NCEP recommendations.

The background and the scientific rationale for
treatment of elevated serum cholesterol are presented
by Drs Cox and Reddy in the first article. They review
the evidence from genetic, experimental,
epidemiological, and clinical studies linking cholesterol
with CHD. The second article by Drs Leyser and
Kucenta discusses the diagnosis and evaluation of
hypercholesterolemia including the classification of

Cholesterol and

CORONARY

HEART

DISEASE

20 JOURNAL VOL 140 MAY

hyperlipoproteinemias. This is followed by an article
by Dr Lopez and Ms Legardeur on the new guidelines
for the treatment of hyperlipidemia. These guidelines,
based on the recommendations of the NCEP, provide
a detailed set of recommendations to guide clinical
practice. The problem of dietary treatment of hyper-
cholesterolemia is
addressed by Ms
Legardeur and Dr
Lopez who give
practical approach-
es to dietary ther-
apy. The final arti-
cle by Dr Levine
focuses on drug
therapy and pro-
vides clear guide-
lines on the selec-
tion and use of
pharmacologic
agents for serum
cholesterol re-
duction.

With the launch-
ing of the NCEP,
preventive cardio-
logy has come of
age and elevated
serum cholesterol
has taken its right-
ful place in public
awareness along-
side high blood
pressure and cigar-
ette smoking. It is
inevitable that as
new knowledge ac-
cumulates, we will
make further pro-
gress in our fight
against CHD. ■

C. Pratap Reddy, MD

LSU School of Medicine,
Shreveport

JOURNAL VOL 140 MAY 21

Consider the
causative organisms...

cefaclor

250-mg Pulvules® t.i.d.
offers effectiveness against
the major causes of bacteriai bronchitis

Haemophilus influenzae and Streptococcus pneumoniae

(ampicillin-susceptible and ampicillin-resistant)

Note: Ceclor is contraindicated in patients with known allergy Penicillin is the usual drug of choice in the treatment and
to the cephalosporins and should be given cautiously to prevention of streptococcal infections, including the prophy-
penicillin-allergic patients. laxis of rheumatic fever. See prescribing information.

Ceclor* (cefaclor)

Summary. Consult the package literature for
prescribing information.

Indication: Lower res p irator y infections ,
inciuding pneumonia, caused by Streptococcus
pneumoniae, Haemophilus influenzae, and
Streptococcus pyogenes (group A /3 -hemolytic
streptococci).

Contraindication;

Known allergy to cephalosporins.

Warnings:

CECLOR SHOULD BE AOtifllNISTERED CAUTIOUSLY TO
PENICILLIN-SENSITIVE PATIENTS. PENICILLINS AND CEPHA-
LOSPORINS SHOW PARTIAL CROSS-ALLERGENICITY. POSSI-
BLE REACTIONS INCLUDEANAPHYLAXIS.

Administer cautiously to allergic patients.
Pseudomembranous coiitis has been
reported with virtually all broad-spectrum anti-
biotics. It must be considered in differential
diagnosis of antibiotic-associated diarrhea.
Colon flora is altered by broad-spectrum
antibiotic treatment, possibly resulting in
antibiotic-associated colitis.

Precautions;

• Discontinue Ceclor in the event of allergic
reactions to it.

• Prolonged use may result in overgrowth of
nonsusceptible organisms.

• Positive direct Coombs' tests have been re-
ported during treatment with cephalosporins.

• Ceclor should be administered with caution in
the presence of markedly impaired renal func-
tion. Although dosage adjustments in moderate
to severe renal impairment are usually not
required, careful clinical observation and labo-
ratory studies should be made.

• Broad-spectrum antibiotics should be pre-
scribed with caution in individuals with a his-
tory of gastrointestinal disease, particularly
colitis.

• Safety and effectiveness have not been deter-
mined in pregnancy, lactation, and infants less
than one month old. Ceclor penetrates mother's
milk. Exercise caution in prescribing for these
patients.

Adverse Reactions: (percentage of patients)
Therapy-related adverse reactions are
uncommon. Those reported include:

• Gastrointestinal (mostly diarrhea): 2.5%.

• Symptoms of pseudomembranous colitis may
appear either during or after antibiotic treat-
ment.

• Hypersensitivity reactions (including mor-
billiform eruptions, pruritus, urticaria, and
serum-sickness-like reactions that have
included erythema multiforme [rarely, Ste-
vens-Johnson syndrome] or the above skin
manifestations accompanied by arthritis/
arthralgia and, frequently, fever): 1 .5%; usually
subside within a few days after cessation of
therapy. Serum-sickness-like reactions have
been reported more frequently in children than
in adults and have usually occurred during or
following a second course of therapy with
Ceclor. No serious sequelae have been
reported. Antihistamines and corticosteroids
appear to enhance resolution of the syndrome.

• Cases of anaphylaxis have been reported, half
of which have occurred in patients with a his-
tory of penicillin allergy.

•As with some penicillins and some other
cephalosporins, transient hepatitis and chole-
static jaundice have been reported rarely.

• Rarely, reversible hyperactivity, nerv-

ousness, insomnia, confusion, hypertonia,
dizziness, and somnolence have been reported.

• Other: eosinophilia, 2%; genital pruritus or
vaginitis, less than 1%; and, rarely, throm-
bocytopenia.

Abnormalities in laboratory results of uncertain
etiology

• Slight elevations in hepatic enzymes.

• Transient fluctuations in leukocyte count
(especially in infants and children).

• Abnormal urinalysis; elevations in BUN or
serum creatinine.

• Positive direct Coombs' test.

• False-positive tests for urinary glucose with

Benedict's or Fehling's solution and ClinitesF
tablets but not with Tes-Tape* (glucose
enzymatic test strip, Lilly). [ositbtli

PA 0709 AMP

Addiliona I information agitable to the
profession on request from EliLitlyand
Company, Indianapolis, Indiana A6285

Eli Lilly Industries, Inc

Carolina, Puerto Rico 00630

CHOLESTEROL AND CORONARY
ATHEROSCLEROSIS

JAMES W. COX JR, MD; C. PRATAP REDDY, MD

Coronary heart disease (CHD) is the leading cause
of death in the United States, accounting for more
than 25% of all deaths.^ A major primary risk
factor for CHD is elevated serum cholesterol level.

Although the association between
hypercholesterolemia and CHD has been
recognized for many years, only recently has it
been established that a reduction in serum
concentration of cholesterol is accompanied by a
decreased risk for CHD. An abundance of genetic,
experimental, epidemiologic, and clinical data
provide conclusive evidence for a causal
relationship between serum cholesterol and
atherosclerotic coronary artery disease. It is the
purpose of this article to review the evidence for
cholesterol and the atherosclerosis connection and
briefly discuss the pathogenetic mechanisms of

atherosclerosis.

G enetic studies in patients with familial hyper-
cholesterolemia provide the most persuasive
evidence for the role of cholesterol in atherosclerosis.^
Familial hypercholesterolemia occurs because of ab-
normalities in gene encoding for low density lipopro-
tein (LDL) receptors. In patients with this inherited
disorder, deficiency of LDL receptor function leads to
accumulation of cholesterol in the plasma and results
in premature atherosclerotic coronary artery disease.
Normally, one functional gene from each parent is
inherited for LDL receptors. Patients with heterozy-
gous form of famUial hypercholesterolemia inherit one
normal gene and one nonfunctioning gene for LDL
receptors, and thus, possess only half the normal
number of LDL receptors. In the homozygous form
of familial hypercholesterolemia, there is an absolute
deficiency of LDL receptors because abnormal genes
are inherited from both parents. One in 500 persons
have heterozygous form of familial hypercholestero-
lemia; homozygous form is much less commonly seen.
Both forms of disease are associated with very high
levels of serum cholesterol and premature athero-
sclerotic vascular disease, but the most fulminant form
of occlusive vascular disease occurs in patients with

JOURNAL VOL 140 MAY 23

the homozygous form of hypercholesterolemia. It is
thought that the most commonly occurring forms of
hypercholesterolemia probably represent a variety of
gene defects that become phenotypically expressed
only in the presence of certain environmental factors.

EXPERIMENTAL STUDIES

In 1913, on the basis of his animal experiments, An-
itschkow proposed that hypercholesterolemia leads
to atherosclerosis.^ He showed that a diet of pure
cholesterol fed to rabbits would lead to hypercholes-
terolemia and atherosclerosis of the coronary arteries
and the aorta. Subsequent studies conducted in many
animal species including non-human primates have
shown that hypercholesterolemia and atherosclerosis
can be produced by feeding diets rich in saturated
fats and cholesterol or containing bile acids. Several
investigators have studied the experimental induction
of atherosclerosis in cynomolgus macaques and rhe-
sus monkeys by feeding a cholesterol rich diet.^ In
these animals, atherosclerosis occurs only when high
levels of serum cholesterol have been achieved, and
early atherosclerotic lesions are seen in the aorta, and
the carotid and iliac arteries. It has been noted that
one rhesus monkey per 300 monkeys at risk per year
may develop a myocardial infarction, a rate similar to
that seen in American men. Also similar to man is
the degree of coronary artery atherosclerosis at each
level of plasma cholesterol concentration.

EPIDEMIOLOGIC STUDIES

Several epidemiologic studies of CHD including one
in Japanese men living outside Japan^ and autopsy
findings in young American soldiers killed in action
during the Korean war^ have strongly suggested a
link between diet, hyperlipidemia, and CHD. How-
ever, it was only recently that convincing evidence
for a direct association between hypercholesterolemia
and CHD was provided by prospective population
studies. The two most notable studies in this regard
are the Framingham Study^ and the Multiple Risk
Factor Intervention Trial (MRFIT) Study.®

THE FRAMINGHAM STUDY

The Framingham Study^ demonstrated a direct cor-
relation between cholesterol levels and mortality from
cardiovascular disease. This conclusion was based on

24 JOURNAL VOL 140 MAY

the results of a 30 year follow-up study carried out in
1,959 men and 2,415 women between 31 and 65 years
of age who were free of cardiovascular disease. In this
study, cardiovascular death increased by 9% for each
10 mg/dl increase in serum cholesterol.

THE MULTIPLE RISK FACTOR
INTERVENTION TRIAL STUDY

The MRFIT Study,® constituting the largest cohort with
standardized serum cholesterol measurements and
long term mortality follow up, showed a “continuous,
graded and strong" correlation between serum cho-
lesterol and CHD death rates. The MRFIT Study in-
cluded 356,222 men between 35 and 57 years of age
who were followed for six years. The mortality rate
due to CHD was 3.5 times higher in patients with
serum cholesterol levels greater than 245 mg/dl when
compared to patients with serum levels of less than
181 mg/dl.

CLINICAL STUDIES

Although the strong association between cholesterol
and coronary heart disease has been recognized for
many years, very little was done about it because
there was no universally acceptable proof that low-
ering the serum cholesterol would reduce the risk of
CHD. A number of recent studies have provided most
compelling evidence that reducing blood cholesterol
levels can lower the risk of CHD. These studies dem-
onstrated that lowering of serum cholesterol not only
decreases incidence of coronary artery disease but may
also slow or arrest the progression of atherosclerotic
lesions.

THE LIPID RESEARCH CLINICS
CORONARY PRIMARY PREVENTION
(LRC-CPP) TRIAL

The LRC-CPP TriaP was a randomized, placebo con-
trolled, double-blind study with two end points being
heart attack and cardiac death. In this study, 3,806
men with a serum cholesterol level of greater than
265 mg/dl and no evidence of coronary artery disease
were randomized into two groups. One group was
treated with low cholesterol diet and cholestyramine
resin and the other with diet plus placebo. All patients
were followed for a minimum of seven years. At the
end of the study period, the treatment group, com-

pared to the placebo group, showed an 8% decrease
in total cholesterol and 11% decrease in LDL choles-
terol; this lowering of cholesterol resulted in 24% re-
duction in cardiac death and 19% decrease in heart
attack.

THE OSLO HEART STUDY

The results of the Oslo Heart Study^° were similar to
those of the LRC-CPP Trial. In this study, 1,232 men
who had no evidence of CHD were placed on cho-
lesterol lowering diet but were not treated with any
cholesterol lowering agents. During the five-year fol-
low-up period, the serum cholesterol level was low-
ered by approximately 13% and the incidence rates
of fatal and nonfatal myocardial infarction and sud-
den death were reduced by 47%. The investigators
estimated that two-thirds of this beneficial effect was
due to lowering of cholesterol and concluded that for
every 1% reduction in serum cholesterol a 2% reduc-
tion in clinical coronary events will occur.

THE NATIONAL HEART, LUNG, AND
BLOOD INSTITUTE (NHLBI) TYPE II
CORONARY INTERVENTION STUDY

The NHLBI Type II Coronary Intervention Study^^
was undertaken to test the hypothesis that lowering
serum LDL cholesterol reduces the rate of progression
of coronary artery disease. In this study, patients with
hypercholesterolemia and coronary artery disease
(CAD) were randomly divided into two groups, one
treated with diet plus cholestyramine and the other
with placebo plus diet. The effect of treatment on the
progression of CAD was evaluated by angiography
which was performed in 116 patients both before and
after five years of treatment. Progression of CAD was
noted in 49% of the placebo group and in only 32%
of the cholestyramine treated group. This difference
was statistically significant.

PATHOGENESIS OF ATHEROSCLEROSIS

Atherosclerosis begins in early childhood and ather-
osclerotic plaques begin to appear at about 20 years
of age. Lesion complications such as ulceration,
thrombosis, and hemorrhage may develop after age
30.

The precise role of cholesterol in atherogenesis
and the cellular mechanisms involved in initiation of
atherosclerosis are not completely understood. At least

three theories — lipid infiltration hypothesis, en-
dothelial injury hypothesis, and monoclonal hypoth-
esis — have been proposed. Currently, a unifying
hypothesis known as “response to injury" hypothesis
is the most widely accepted. This hypothesis states
that atherosclerosis is initiated in response to injury
to arterial endothelium. Endothelial integrity is main-
tained by both structural and functional components.
Previously it was thought that a mechanical injury to
the endothelium was necessary for initiation of ath-
erosclerotic process. However, recent investigation has
shown that a denuding injury is not essential and that
high levels of lipoprotein may disrupt the functional
integrity of the endothelium without an apparent in-
jury. Experimental studies have revealed several pos-
sible mechanisms by which endothelium may be "in-
jured" as a result of chronic exposure to elevated levels
of LDL cholesterol. Jackson and Gotto^^ have sug-
gested that changes in the cholesterol to phospholipid
ratio of the plasma membranes of cells may lead to
increased membrane viscosity. Such a change might
decrease the malleability of endothelial cells making
them more fragile. Endothelial injury may also occur
as a result of toxic substances released by oxidized
LDL and by foam cells formed from monocytes and
macrophages in response to increased levels of LDL
cholesterol. Hypercholesterolemia may produce a
mitogenic response in smooth muscle cells and in-
crease monocyte adhesion and chemotaxis leading to
proliferation of smooth muscle cells and development
of fatty streaks. Vasomotor changes caused by hy-
percholesterolemia may also be a factor in the path-
ogenesis of atherosclerosis. In rabbits fed a high cho-
lesterol diet, acetylcholine induced endothelium-
dependent relaxation can be diminished or converted
to contraction.^^ Several other factors including plate-
let and endothelial cell derived growth factors and
prostaglandins also appear to play an important role
in the pathogenesis of atherosclerosis.^^ A discussion
of these factors and their regulating mechanisms is
beyond the scope of this article.

SUMMARY

The association of hypercholesterolemia and coronary
heart disease is well established. The mechanisms by
which hypercholesterolemia initiates and propagates
atherosclerosis are not fully understood but are under
active investigation. There is now incontrovertible
proof that reducing serum cholesterol levels will re-

JOURNAL VOL 140 MAY 25

suit in reduced mortality and morbidity from coronary
heart disease. Beneficial effects can be obtained by
both primary prevention in patients with no history
of cardiovascular disease and secondary prevention
in patients with known coronary artery disease. ■

REFERENCES

1. Inter-Society Commission for Heart Disease Resources; Optimal re-
sources for primary prevention of atherosclerotic disease. Circulation
1984;70:153A.

2. Goldstein JL, Brown MS: Regulation of low density lipoprotein receptors:
Implications for pathogenesis and therapy of hypercholesterolemia and
atherosclerosis. Circulation 1987;76(3):504-507.

3. Anitschkow NN: A history of experimentation on arterial atherosclerosis
in animals, in Cowdry's Arterios, ed 2, Blumenthal HT (ed). Springfield,
ni, Charles C Thomas, 1967, p 21.

4. Jokinen MP, Clarkson TB, Prichard RW: Animal models of atheroscle-
rosis research. Exp Mol Pathol 1985;42:1.

5. Robertson TL, Kato H, Gordon T, et al: Epidemiologic studies of coronary
heart disease and stroke in Japanese men living in Japan and Hawaii.
Am } Cardiol 1977;39:244-249.

6. Enos WE, Holmes RH, Beyer J: Coronary disease among United States
soldiers killed in action in Korea. JAMA 1953;152:1090-1093.

7. Anderson KM, CasteUi WP, Levy D: Cholesterol and mortality: 30 years
follow-up from the Framingham Study. JAMA 1987;254:2176-2180.

8. Stamler J, Wentworth D, Neaton JD: Is relationship between serum cho-
lesterol and risk of premature death from coronary heart disease con-
tinuous and graded? Findings in 356,222 primary screenees of the Mul-
tiple Risk Factor Interventional Trial (MRFIT). JAMA 1986;256:2823.

9. Lipid Research Clinics Program, The Lipid Research Clinics Coronary
Primary Prevention Trial Results II. The relationship of reduction in
incidence of coronary heart disease to cholesterol lowering. JAMA
1984;251:365-374.

10. Hjermann I, Velve Byre K, Holme I, et al: Effect of diet and smoking on
the incidence of coronary heart disease: Report from Oslo Study Group
of a randomized trial in healthy men. Lancet 1981;2:1303-1310.

11. Levy RI, Brensike JF, Epstein SE, et al: The influence of changes in lipid
values induced by cholestyramine and diet on progression of coronary
artery disease: Results of the NHLBI Type II coronary intervention study.
Circulation 1984;69:325.

12. Ross R; The pathogenesis of atherosclerosis — an update. N Engl J Med
1986;314:488.

13. Jackson RL, Gotto AM Jr: Hypothesis concerning membrane structure,
cholesterol, and atherosclerosis, in Atherosclerosis Reviews, Padetti R, Gotto
AM Jr (eds). New York, Raven Press, 1976, vol 1, pp 1-21.

14. Cathcart MK, Morel DW, Chisolm GM III: Monocytes and neutrophils
oxidize low density lipoprotein making it cytotoxic. J Leukocyte Biol
1984;38:341-350.

15. Ibeugwe JK, Susuki H: Protective action of elastase on changes in me-
chanical properties of vascular smooth muscles during atherosclero-
genesis in hypercholesterolemic rabbits. Arch Int Pharmacodyn Ther
1987;287:48-64.

16. Clarkson TB, Weingand KW, Kaplan OR, et al; Mechanisms of athero-
genesis. Circulation 1987;76 (suppl 1), 1-20.

Dr Cox, a fellow in cardiology, is affiliated with the Dept of Medicine,
Cardiology Section, at LSU School of Medicine in Shreveport.

Dr Reddy, a professor of medicine, is the associate chief of cardiology at

LSU School of Medicine in Shreveport.

Reprint requests should be sent to C. Pratap Reddy, MD, Professor of
Medicine, Cardiology Section, LSU School of Medicine, PO Box 33932,

Shreveport, LA 70113.

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26 JOURNAL VOL 140 MAY

DIAGNOSIS AND EVALUATION OF
HYPERCHOLESTEROLEMIA

LARRY J. LEYSER, MD; BRYAN LUCENTA, MB

The primary lipids in plasma are cholesterol and
triglycerides. Cholesterol is an essential component
in cellular metabolism, and triglycerides are an
important source of energy. Although vital to the
functioning of many of the body's tissues, the
lipids are insoluble in water and must be
transported to cells by other molecules. These
transporting molecules, complex macromolecular
aggregations of lipid and protein, are known as
lipoproteins. Abnormalities in the synthesis and
degradation of plasma lipoproteins are related to
disorders of lipoprotein metabolism. The hallmark
of lipoprotein disorders is hyperlipidemia or the
elevation of plasma cholesterol and/or triglyceride
concentrations. These abnormalities may result
from primary inborn errors of metabolism or may
be secondary to a variety of other disease states.^
The purpose of this article is to review the
classification, diagnosis, and evaluation of
lipoprotein disorders.

T he four major lipoprotein classes are defined ac-
cording to their density on ultracentrifugation. ^

1. Chylomicrons. These transport dietary fat (as
triglycerides) and a small amount of cholesterol from
the intestine to the plasma. The triglycerides are re-
moved by lipoprotein lipase and stored in fat cells as
fatty acids. A remnant remains which, unless re-
moved by the Uver, is thought by some investigators
to have an atherogenic capability similar to thaf of
low-density lipoproteins.

2. Very low density lipoproteins (VLDL). These are
secreted by the liver and they transport triglycerides
and a small amount of cholesterol. Lipoprotein lipase
removes triglycerides from VLDL which are then me-
tabolized in the liver with low-density lipoprotein as
the end product.

3. Low-density lipoproteins (LDL). These are the
end product of VLDL metabolism, and some LDL is
secreted directly into the plasma. Low-density lipo-
proteins are the major carriers of cholesterol and are
closely linked to atherogenesis. The amount of LDL
taken up by the cells is controlled by LDL "receptors"
located on the ceU membrane and deficiency of these
receptors results in elevated levels of plasma LDL
cholesterol.

JOURNAL VOL 140 MAY 27

TABLE 1

CLASSIFICATION AND CHARACTERISTICS OF HYPERLIPOPROTEINEMIAS

Major Elevation in Plasma

Phenotype

Genotype

Lipoprotein

Lipid

Familial Hyperchylomicronemia

Chylomicrons

Triglyceride

lla

Familial Hypercholesterolemia (homozygous or heterozygous)

LDL*

Cholesterol

Familial Combined Hyperlipidemia

LDL

Cholesterol

Polygenic Hypercholesterolemia

LDL

Cholesterol

Familial Hypercholesterolemia

LDL

Cholesterol

Familial Combined Hyperlipidemia

VLDLt

Triglyceride

III

Familial Dysbetalipoproteinemia

IDLt

Cholesterol

Triglyceride

Familial Hypertriglyceridemia

VLDL

Triglyceride

Familial Combined Hyperlipidemia

LDL

Cholesterol

Familial Type V

Chylomicrons

Triglyceride

Familial Hypertriglyceridemia

VLDL

Cholesterol

* Low density lipoprotein
t Very low density lipoprotein
t Intermediate density lipoprotein

4. High-density lipoproteins (HDL). These are the
second major carrier of cholesterol and are thought
to be responsible for the transport of cholesterol to
the liver for secretion in the bile. High levels of HDL
are thought to be protective against atherosclerosis.

DEFINITION OF HYPERLIPIDEMIA

Traditionally, hyperlipidemia has been diagnosed
when a person's serum cholesterol or triglyceride lev-
els exceeded the 95th percentile for his (her) age and
sex. This definition has been revised and new guide-
lines for the diagnosis of hypercholesterolemia have
been provided by the National Institutes of Health
Cholesterol Consensus Development Conference.^

RISK FOR CORONARY HEART
DISEASE

Atherosclerosis and coronary heart disease are strongly
associated with increased plasma cholesterol levels,
and the degree of risk for coronary heart disease is

directly related to the patient's plasma lipid levels.
For determining such risk one must adhere to the
National Cholesterol Education Program recommen-
dations.^ According to these recommendations, a
serum cholesterol level of less than 200 mg/dl carries
no risk for coronary heart disease, a level between
200 mg/dl and 230 mg/dl carries minimal risk, and a
level of equal to or greater than 240 mg/dl carries high
risk. Hypertriglyceridemia is present when triglyc-
eride levels exceed 250 mg/dl; triglyceride concentra-
tions of greater than 500 mg/dl are considered high
while levels between 250 mg/dl and 500 mg/dl are
considered borderline high.

CLASSIFICATION OF
HYPERLIPOPROTEINEMIAS

In many patients, hyperlipoproteinemia is the result
of overconsumption of dietary fat, but in others this
may be genetically determined. Some of these dis-
orders arise from inherited defects. The most common
of these are polygenic hypercholesterolemia, endog-

28 JOURNAL VOL 140 MAY

enous hypertriglyceridemia, familial hypercholester-
olemia, and familial combined hyperlipidemia. A less
common type is mixed hyperlipidemia.

HyperUpoproteinemias are classified on the basis
of the specific lipoprotein represented in the increased
plasma lipid values. This classification (Table 1) de-
vised by Fredrickson et al^ is based on laboratory
measurements of lipoproteins but is useful in making
certain clinical correlations.

SECONDARY HYPERLIPIDEMIA

In some patients, hyperlipidemia may be secondary
to another disease, a metabolic disorder, or to the use
of certain drugs. These causative factors are listed in
Table 2. The hypercholesterolemia due to these etiol-
ogies can usually be modified by treatment of the
disease process, correction of the metabolic abnor-
mality, or discontinuation of the drug eliciting the
abnormality.

CLINICAL MANIFESTATIONS

Hypercholesterolemia presenting as increased LDL
cholesterol and normal triglyceride levels can be found
in familial hypercholesterolemia, familial combined
hyperlipidemia, and polygenic hypercholesterolemia.
Elevated cholesterol also occurs with broad beta dis-
ease (type III hyperlipoproteinemia) and lipoprotein
lipase deficiency.

Familial hypercholesterolemia is transmitted as
an autosomal dominant trait with both homozygous
and heterozygous forms and is characterized by in-
creased LDL cholesterol and normal or mildly ele-
vated plasma triglyceride levels. The patient with the
homozygous form of disease presents early in child-
hood with planar, tuberous, and tendon xanthomas.^
Planar xanthomas are recognized as yellow lesions in
the finger web spaces and behind the knees. The het-
erozygous form of this disorder has lower levels of
plasma cholesterol (280 mg/dl to 550 mg/dl) and may
not present with tendon xanthomas until later in life.
The xanthomas are due to insidious deposition of LDL
cholesterol in the skin and tendons. These patients
have accelerated atherosclerotic cardiovascular dis-
ease and may present with valvular and supravalvular
stenosis, and early myocardial infarction. Diagnosis
of familial forms can be made by skin biopsies and
skin fibroblast studies.

Familial combined hyperlipidemia is an autoso-

TABLE 2

CAUSES OF SECONDARY HYPERLIPOPROTEINEMIA

Hypothyroidism
Diabetes mellitus
Nephrotic syndrome
Obstructive liver disease
Glycogen storage disease
Myelomas

Cushing’s syndrome
Hyperuricemia

mal dominant inherited disorder characterized by an
overproduction of VLDL and LDL by the Ever. One
may see a type Ila phenotype (increased LDL choles-
terol), type Ilb phenotype (increased VLDL and LDL
cholesterol) or a type IV phenotype (singular eleva-
tion of VLDL cholesterol). Tendon xanthomas are in-
variably absent in this disorder but eruptive xantho-
mas may occur in those with hypertriglyceridemia
and diabetes mellitus. The laboratory diagnosis is made
by demonstration of different lipoprotein phenotypes
in different family members.

Combined hypercholesterolemia and hypertri-
glyceridemia occurs in type lib phenotypes with el-
evated LDL and VLDL, or may indicate the presence
of abnormal chylomicron and VLDL remnants that
are typical of dysbetalipoproteinemia (type III hyper-
lipoproteinemia). To differentiate between type lib
and type III, one must use ultracentrifugal separation
of the VLDL component. Clinically, these patients
have palmar and tuberous xanthomas, and tubero-
eruptive xanthomas on the buttocks. There is an in-
creased incidence of coronary and peripheral vascular
disease thought to be caused by the uptake of VLDL
and LDL cholesterol by the arterial smooth muscle
cells and macrophages. This disorder is usually as-
sociated with obesity, diabetes meUitus, hypothy-
roidism, or a coexistent familial hyperlipidemia.

EVALUATION

For the determination of serum lipid levels, blood
samples should be obtained from the patient after a
12-hour fast. Total serum cholesterol, triglycerides,
and HDL levels should be measured during the initial
screening. If the values are normal at initial screening.

JOURNAL VOL 140 MAY 33

they should be repeated every five years. If an ab-
normality is found at initial evaluation, this should
be confirmed by a second test followed by identifi-
cation of the underlying lipoprotein abnormality. The
level of LDL cholesterol can be deduced by using the
following formula developed by the Lipid Research
Clinics Program: LDL cholesterol = total cholesterol
— HDL cholesterol — triglyceride level/5. ■

REFERENCES

1. Havel RJ, et al: Lipoprotein and lipid transport, in Metabolic Control and
Disease, ed 8, Bondy PK, Rosenberg LE (eds). Philadelphia, W.B. Saun-
ders, 1980, chap 7, pp 393-494.

2. Peters WL, Goroll AH: The evaluation and treatment of hypercholester-
olemia in primary care practice. / Gen Intern Med 1986;1(3):183-195.

3. Consensus Conference [National Institutes of Health Cholesterol Con-
sensus Development Conference]: Lowering blood cholesterol to prevent
heart disease. JAMA 1985;253:280.

4. Lipid Research Clinics Program: The Lipid Research Clinics — Coronary
Primary Prevention Trial (CPPT) Results. I. Reduction in incidence of
coronary heart disease to cholesterol lowering. II. The relationships or
reductions in incidence of coronary heart disease to cholesterol lowering.
JAMA 1984;251:351.

5. Fredrickson DS, Levy RI, Lees RS: Fat transport in lipoproteins — an
integrated approach to mechanism and disorders. N Engl J Med 1967;276:34-
281.

6. Weidman W, Kwiterovich Jr P: Diagnosis and treatment of primary hy-
perlipidemia in childhood. Circulation 1986;74:1181A-1188A.

Dr Leyser is assistant professor of medicine in the Dept of Medicine,
Cardiology Section, at LSU School of Medicine in New Orleans.

Dr Lucenta, a fellow of cardiology, is also affiliated with the Dept of
Medicine, Cardiology Section, at LSU School of Medicine in

New Orleans.

Reprint requests should be sent to Jjirry J. Leyser, MD, LSU School of
Medicine, Dept of Medicine, Section of Cardiology, 1542 Tulane Ave,

New Orleans, LA 70112.

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34 JOURNAL VOL 140 MAY

NEW GUIDELINES
FOR THE TREATMENT OF
HYPERLIPIDEMIA IN ADULTS

ALFREDO LOPEZ-S, MD, PhD; BARBARA Y. LEQARDEUR, MPH

High blood cholesterol values have been shown to
be a major risk factor for coronary heart disease. In
an attempt to diminish this risk, newly developed
guidelines have been proposed by the National
Heart and Lung Institute in cooperation with the
American Heart Association and other health
organizations. To educate physicians in the
detection, evaluation, and treatment of individuals
with elevated blood cholesterol levels, it is
recommended that all adults over 20 years of age
be tested for their serum cholesterol levels as part
of a regular evaluation of risk factors. Step-wise
recommendations are given for the evaluation and
treatment of those individuals found to be at risk
because of their serum cholesterol values.

C ORONARY HEART DISEASE (CHD) continues to be
the major cause of death in the United States,
and Louisiana is a state with one of the highest death
rates for the disease.^ Hypercholesterolemia is one of
the major risk factors of this disease and there is evi-
dence of high incidence of hyperlipidemia in the Lou-
isiana population. 2 The participants of the Consensus
Conference on Lowering Blood Cholesterol to Prevent
Coronary Heart Disease, sponsored by the National
Institutes of Health (NIH), agreed that the cause-and-
effect relationship between blood cholesterol and CHD
is related, that a decline in CHD mortality in the United
States can be effected by control of hypercholestero-
lemia, and that the National Heart, Lung and Blood
Institute (NHLBI) should mount a national cholesterol
education program for both physicians and the pub-
lic.^ As a result of their recommendations, the NIH
and the American Heart Association (AHA), along
with multiple other cooperating governmental,
professional, and voluntary health organizations have
launched an ambitious project — the National Cho-
lesterol Education Program. It is aimed at educating
physicians and the general public regarding hyper-
cholesterolemia. For this purpose, simple guidelines ^

JOURNAL VOL 140 MAY 35

Fig. Guidelines for the treatment of hyperlipidemia
in adults.

have been developed for screening, diagnosis, and
treatment of individuals at different levels of risk based
on their cholesterol values and the presence or ab-
sence of other risk factors for CHD (Fig). These guide-
lines are compatible with recently developed methods
that allow fast (three to eight minutes) measurement
of cholesterol levels in small amounts of blood (10-20
fxl obtained by finger stick) and new information re-

garding the benefits of diet and drug therapy in the
treatment of hyperlipidemia.

DETECTION AND CLASSIFICATION OF
SERUM CHOLESTEROL

The AHA endorsed the recommendation that aU adults
over age 20 should be tested for their serum choles-
terol, which can be obtained in a fasting or non-fasting
state.

Individuals with total serum cholesterol less than
200 mg/dl are considered to have "desirable blood
cholesterol," and are encouraged to follow the AHA
diet and lead a healthy lifestyle. They should have
their serum cholesterol repeated in five years.

When the serum cholesterol level is 200 mg/dl, it
needs to be confirmed by a new determination in one
to eight weeks. If this confirmation value is within 30
mg/dl of the first one, the average of the two tests is
used for decisions following the guidelines. If the sec-
ond value differs from the first by more than 30 mg/
dl, a third determination should be made in another
one to eight weeks and the three values averaged. If
this averaged value of cholesteroTis between 200 mg/
dl and 239 mg/dl, the value is called "borderline high
total cholesterol," and if it is above 240 mg/dl, the
value is called “high total cholesterol." In those in-
dividuals with borderline high (200 mg/dl to 239 mg/
dl) value of cholesterol, their risk factor status should
be evaluated. A "high risk" status is defined accord-
ing to the AHA guidelines as the presence of definite
CHD or two other risk factors. The risk factors for
CHD include: 1) male sex, 2) family history of pre-
mature CHD, 3) cigarette smoking, 4) hypertension,
5) low HDL-cholesterol (<35 mg/dl), 6) diabetes mel-
litus, and 7) severe obesity (>30% overweight).

Those other individuals with "borderline high"
serum cholesterol (200 mg/dl to 239 mg/dl) but with-
out CHD or two risk factors, do not require special
treatment, and are advised to follow the AHA diet
along with a healthy lifestyle. Educational material
should be given to them, and their serum cholesterol
should be repeated in one year.

If the patient has borderline high cholesterol and
is at high risk (presence of CHD or two risk factors),
lipoprotein analysis needs to be performed.

In patients with "high total serum cholesterol"
(over 240 mg/dl), lipoprotein analysis needs to be per-
formed. The ultimate classification of a patient's cho-

36 JOURNAL VOL 140 MAY

lesterol status will be based on the low density lipo-
protein (LDL)-cholesterol level.

DETERMINATION AND
CLASSIFICATION OF LDL
CHOLESTEROL

Determination. To determine LDL cholesterol it is nec-
essary to order a 12-hour fasting lipid analysis con-
sisting of total cholesterol, high density lipoprotein
(HDL)-cholesterol, and triglycerides. From the results
of this test, LDL-cholesterol can be calculated as fol-
lows:

LDL-cholesterol = Total cholesterol —
(HDL-cholesterol + triglycerides/5)

It is advisable to perform two or three determi-
nations, one to eight weeks apart and establish an
average LDL-cholesterol level.

Classification. A desirable LDL-cholesterol is be-
low 130 mg/dl. Individuals with “desirable" LDL-cho-
lesterol levels are advised to repeat total cholesterol
level in five years and to follow the AHA diet and to
lead a healthy lifestyle.

Borderline high-risk LDL-cholesterol is an LDL-
cholesterol level of 130 mg/dl to 159 mg/dl. For indi-
viduals with borderline high risk LDL-cholesterol lev-
els and evidence of CHD or two risk factors, it is
recommended that they follow the Step I diet and
have their cholesterol reevaluated annually.

Those individuals with borderline LDL-choles-
terol values and presence of CHD or two risk factors
should be treated the same as individuals with high
risk LDL-cholesterol.

High risk LDL-cholesterol is a level of over 160 mg/
dl. These individuals require a complete clinical eval-
uation to determine secondary or genetic causes for
their hyperlipidemia and should enter a cholesterol-
lowering therapy (diet alone or diet plus drugs) in
order to achieve an LDL-cholesterol level of less than
160 mg/dl when no CHD risk factors are present and
a level of less than 130 mg/dl in the presence of def-
inite CHD or two other risk factors.

SUMMARY

According to the new guidelines of the NHLBI and
AHA, cholesterol determinations should be done in
all adults over 20 years of age. On the basis of cho-

lesterol level and the presence or absence of CHD or
two other risk factors, individuals will be classified as
having desirable, borderline-high, or high-risk cho-
lesterol levels. A decision to start a patient on active
medical therapy for high cholesterol levels should be
made on the basis of the LDL-cholesterol classifica-
tion, not the serum total cholesterol. ■

REFERENCES

1. Oalman MC: Coronary Heart Disease in Louisiana. / La State Med Soc
1974;126:39.

2. Lopez-S A: Coronary Heart Disease Detection Program. / La State Med Soc
1974;126:43.

3. NIH Consensus Development Conference Summary. JAMA
1985;253(14);2080.

Dr. Lopez-S is a professor of medicine in the Dept of Medicine,
Nutrition Section, at LSU School of Medicine in New Orleans.

Ms Legardeur is a registered dietitian and an assistant professor of
clinical medicine in the Dept of Medicine, Nutrition Section, at
LSU School of Medicine in New Orleans.

Reprints will not be available.

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JOURNAL VOL 140 MAY 37

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38 JOURNAL VOL 140 MAY

DIETARY TREATMENT OF
ELEVATED SERUM CHOLESTEROL

BARBARA Y. LEGARDEUR, MPH; ALFREDO LOPEZ-S, MD, PhD

Diet is essential to the management of high blood
cholesterol in patients. Dietary factors which
contribute to increased serum cholesterol levels
include a high intake of saturated fatty acids, a
relatively high intake of cholesterol, and obesity.
A two-step diet approach has been developed by
members of the National Cholesterol Education
Program and the American Heart Association. This
two-step approach progressively reduces the intake
of saturated fatty acids and dietary cholesterol, as
well as controlling the level of calories, if
warranted. Physicians are advised to become
knowledgeable of the Step 1 Diet and to
implement it in appropriate patients. The major
components of the Step 1 Diet include limitation
of meat, fish, and poultry, up to 6 oz daily; use of
low-fat dairy products, no more than three egg
yolks per week; and up to 6 to 8 teaspoons of fats
and oils daily. The guidelines also recommend
increased use of fruits, vegetables, and grain

products in the diet.

D iet is the cornerstone of management for the per-
son with high or borderline high blood choles-
terol. For many people, this will necessitate perma-
nent changes in eating behavior rather than temporary
modification of food intake. The factors in the Amer-
ican diet that contribute to increased serum choles-
terol levels are a high intake of saturated fatty acids,
relatively high intake of dietary cholesterol, and ex-
cess calories that exceed the body's requirement re-
sulting in obesity.^

DIETARY FAT

In the average American diet, approximately 13% to
15% of total calories come from saturated fatty acids.

It is estimated that the proportion of saturated fatty
acids in the average Louisianan diet is similar to that
of the average American diet.^'^ In general, animal
fats (butter, beef and pork fat) contribute most of the
saturated fatty acids to diet but a significant portion
may come from certain vegetable oils (palm, palm
kernel, and coconut oil).

The polyunsaturated fatty acids, especially lino-
leic acid, have been shown to lower serum cholesterol
when substituted for saturated fatty acids. However, ^

JOURNAL VOL 140 MAY 39

Cholesterol

(mg/IOOgm

food)t

Total Fat
(g/100gm
food)

Red Meats

Beef (average)

10-15

Lamb (average)

10-15

Pork (average)

10-15

Veal (average)

Organ meats

Liver, beef

320

Pancreas (sweetbreads)

280

Kidney

300

Brains

1810

Poultry

Chicken (without skin)

light

dark

Fish

Flounder

Trout, brook

Tuna

Shellfish

Crab

Crayfish

1.5

Lobster

Oyster

Scallop

Shrimp

161

because these lower both the LDL and HDL fractions
of cholesterol and may increase the risk of gallstones/
it is recommended that not more than 10% of dietary
calories should come from polyunsaturated fatty acids.
Sources of polyunsaturated fatty acids include plant
oils such as corn, sunflower, soybean, and safflower.
Previously, monounsaturated fatty acids were thought
to be neutral in their effect on serum cholesterol; how-
ever, recently, these fatty acids, when substituted for
saturated fatty acids in the diet, have been shown to
lower total cholesterol by selectively lowering LDL
fraction.^ Monounsaturated fatty acids are found in
olive oil, rapeseed (canola oil) and other high-oleic
forms of sunflower oil.

Severe reduction (less than 30% of calories as fat)

of total amount of fat in the diet is not necessary for
successful lowering of serum cholesterol provided
saturated fatty acids are reduced.^ For obese patients,
the decrease in total fat will facilitate weight reduc-
tion.

DIETARY CHOLESTEROL

The second factor which contributes to increased
serum cholesterol levels is a relatively high intake of
cholesterol. The average American diet contains ap-
proximately 350 mg to 450 mg of cholesterol a day.^
Dietary cholesterol will increase serum cholesterol
levels by approximately 4 mg/dl per 100 mg choles-
terol.^ Although all animal products contain choles-
terol in both the fat and muscle of the animal, the
most concentrated sources of dietary cholesterol are
egg yolk and organ meats (liver, kidney, sweet-
breads). Shrimp contain a moderate amount of cho-
lesterol while other shellfish (oysters, crayfish, and
crabs) contain considerably less (Table 1).

DIETARY CALORIES

The third factor is caloric intake that exceeds body
requirements. Excessive caloric intake may result in
obesity, may lead to an overproduction of very low
density lipoprotein (VLDL) and thus, an increase in
low density lipoprotein (LDL) levels.^ Obesity may
also lower the high density lipoprotein (HDL) fraction
of cholesterol. Loss of body weight may not only fa-
vorably influence serum cholesterol levels but may
also decrease triglyceride levels in persons with hy-
pertriglyceridemia .

DIETARY THERAPY OF HIGH BLOOD
CHOLESTEROL AND BORDERLINE
HIGH CHOLESTEROL

The American Heart Association and National Cho-
lesterol Education Program have designed a two-step
approach for the modification of diet for elevated cho-
lesterol levels. This approach, outlined in Table 2, is
designed to progressively reduce intake of saturated
fatty acids and dietary cholesterol and to eliminate
excess calories, if necessary. The Step 1 Diet, as de-
scribed below, is prescribed by the physician and im-
plemented by the physician and the immediate staff.
The patient's serum cholesterol should be measured
at four to six weeks and at three months following

40 JOURNAL VOL 140 MAY

Recommended Intake

Nutrient

Step 1

Step 2

Total fatf

less than 30% of calories

Saturated fatty acids

< 1 0% of calories

<7% of calories

Polyunsaturated fatty acids

up to 1 0% of calories

Monounsaturated fatty acids

1 0% to 1 5% of calories

Cabohydrates

50% to 60% of calories

Protein

1 0% to 20% of calories

Cholesterol

<300 mg/day

<200 mg/day

Total Calories

To achieve and maintain

desirable weight

initiation of Step 1 . If there is not sufficient reduction
of serum cholesterol at the end of three months, Phase
2 should be initiated with the assistance of a registered
dietitian. As noted in Table 2, Phase 2 is lower in
dietary cholesterol and saturated fatty acids. Al-
though the response rate to the diet is variable and
depends on the previous diet, it has been estimated
that changing from the typical American diet to the
Step 1 diet will result in an average decline of 30 mg/
dl to 40 mg/dl in serum cholesterol. Progressing to
Step 2 should result in an additional decrease of 15
mg/dl in serum cholesterol.^

EVALUATION OF PATIENT'S
CURRENT DIET

An assessment of past dietary intake provides a foun-
dation from which to direct modification of a patient's
eating behavior. Evaluation of diet will allow the ed-
ucator to focus on problem areas and prevent dupli-
cation of current knowledge. A recent report® indi-
cated that while the general US population could
identify primary sources of polyunsaturated fatty acids
and saturated fatty acids, only 32% correctly re-
sponded to the statement cholesterol is found in an-
imal products. Questions which may be of help in
evaluating the current diet are summarized in Table
3.

Frequency and type of milk consumed.

Use and frequency of high-fat cuts of meat used in preparation
of vegetables, beans, and stews.

Use and frequency of egg yolks and organ meats.

Frequency and type of cheese consumed.

Type of fat/oil used in cooking and as spread.

Frequency and selection of convenience, processed, or fast foods.
Cuts and amounts of meat consumed.

RECOMMENDED PATTERN FOR
STEP 1 DIET (Table 4)

Meats, Poultry, and Fish

Meat consumption is limited to 6 oz of lean meat (beef,
pork, veal, and lamb), skinless poultry and fish. Table
1 lists fat and cholesterol content of these items. Lean
cuts of beef include lean ground beef, rump roast,
and round steak. Severe reduction of red meat is not
advised, especially for premenopausal women, since
meat is rich in iron and protein. Use of skinless chicken
and turkey along with seafood is encouraged. Finfish
and shellfish contain varying amounts of cholesterol,
but are low in saturated fats. The finfish caught in
temperate waters of Louisiana are generally lowfat ^

JOURNAL VOL 140 MAY 41

TABLE 4

CALORIE-CONTROLLED MEAL PATTERNS FOR STEP 1 DIET

2500

Number of Servings
2000

1200

calories

Lean meats, poultty, seafood

6 oz

Eggs

3 per wk

Dairy Products (lowfat)*

Fatt

Bread, pasta, cereal, starchy vegetables^

Vegetables§

Fruitll

Modified fat dessert

Average amounts:

* 8 oz skim milk
t 1 tsp margarine
t 1 slice bread, 3/4 cup dry cereal
§ 1/2 cup cooked, 1 cup raw
11 1/2 cup, 1 raw fruit

fish (excluding mackerel) as compared to certain spe-
cies found in colder waters. Shrimp contain more cho-
lesterol than other shellfish; however, they may be
included in the diet by reducing the portion size (ie,
3 oz lean meat, chicken or fish = 2 oz shrimp). Some
foods to be avoided include well-marbled meats such
as rib eyes, high fat meats (pickled pork, bacon, etc)
used to flavor vegetables and beans, commercially
fried chicken and fish, and high fat luncheon meats
such as bologna and salami.

Dairy Products

At least two servings of low fat dairy products are
recommended for an adult to maintain calcium intake.
One serving is equal to approximately 8 oz of skim
milk, 1 oz lowfat cheese or 1 c of plain, lowfat yogurt.
Use skim milk or lowfat (1%) milk as opposed to whole
milk which is approximately 3.25% butterfat. In ad-
dition, replace high fat cheeses (such as cheddar,
Swiss, blue, etc) with lowfat cottage cheese (1% to 2%
butterfat) and other cheeses made with skim milk,
such as farmer or ricotta. Although manufacturers
may advise certain cheeses as "lower in fat," the ac-
tual amount should be no more than 2 gm to 6 gm
fat per oz.

Fats and Oils

Reduce fats and oils that are high in saturated fatty
42 JOURNAL VOL 140 MAY

acids or cholesterol. Generally, unsaturated oils are
limited to six to eight servings per day, but the amount
will vary with the level of calories. One serving is
equal to approximately 1 tsp of margarine or oil. De-
sirable vegetable oils include corn, cottonseed, saf-
flower, rapeseed (canola), soybean, or olive. Vege-
table products do not contain cholesterol, but a high
intake will contribute excess calories. Since butter is
high in cholesterol and fat, margarine is the preferred
spread. Use margarines in which the first ingredient
listed on the label is a liquid vegetable oil, and look
for partially hydrogenated oils rather than hydrogen-
ated.

Palm oil, palm kernel oil, and coconut oil are found
in many processed foods, bakery goods, popcorn oils,
and non-dairy creamers and should be avoided since
they are very high in saturated fatty acids.

The number of egg yolks is limited to three per week
including those used in cooking.

Breads, Cereals, Pasta, Rice, Dried Peas, and Beans
These products are good sources of protein and car-
bohydrate and most are low in fat. At least four serv-
ings per day are recommended. One serving of this
group is equal to one slice of bread, two-thirds to

three-fourths cup of ready-to-eat cereal, or one-half
cup of cooked cereal.

French bread, a popular Louisiana bread, con-
tains little fat and is appropriate along with sliced,
hard rolls, pita bread, English muffins, and bread
sticks. Commercially baked goods often contain
shortenings high in saturated fats. Cornbread, bis-
cuits, and other quick breads may be included in the
diet when they are modified to contain appropriate
ingredients (ie, skim milk, margarine, egg whites, or
egg substitutes).

Beans and rice, a mainstay of Louisiana diets, are
an example of complimentary proteins. Many people
will need to adjust their cooking by deleting "high
fat" seasonings and increase vegetable seasonings such
as onion, celery, and green pepper for added flavor.

Fruits and Vegetables

A minimum intake of three servings of fruits and three
servings of vegetables are recommended daily. A usual
serving of fruit is one medium size fruit or one-half
cup of canned fruit, and for vegetables one-half cup
of cooked is considered an average serving. Com-
mercially prepared vegetables with cream, butter, or
cheese sauces should be avoided.

Alcohol

Moderate use of alcohol can be included within the
scope of the recommendations, since it does not affect
LDL concentration. However, it may increase serum
triglyceride levels and HDL-cholesterol in some in-
dividuals.

Food Preparation

Recommended methods include those that require
little or no fat in cooking. Baking, steaming, broiling,
and grilling are preferred to frying. In order to facil-
itate change in a population that often prefers frying
and stewing of their foods, recommending gradual
modification may be advantageous. Desirable vege-
table oils should be used on those occasions when
foods are fried. Reduced fat and appropriate substi-
tutions in stews and gumbos will allow patients to
still enjoy their foods. Soups and stews should be
chilled after cooking, and the congealed fat that forms
on top should be removed prior to serving.

Monitoring

Follow-up and monitoring are important in order to
achieve a long-term change in eating behavior. The

schedule, as proposed by the National Cholesterol
Education Program and outlined in the preceding ar-
ticle "New guidelines for treatment of the hyper-
lipidemia in adults" (Lopez-SA, Legardeur BY), ad-
vises that cholesterol levels be measured at four to six
weeks and three months following initiation of the
Step 1 diet. If the desired response is achieved, this
should be confirmed by measuring LDL-cholesterol.
The patient should then enter a long-term monitoring
program. Long-term monitoring includes measuring
total cholesterol, four times the first year and twice
each year thereafter. Reinforcement of the diet and
behavior is an essential component of long-term mon-
itoring. When the response to the Step 1 diet is in-
adequate, the person should be referred to a regis-
tered dietitian for either retrial of Step 1 diet or for
instruction on Step 2 diet. Cholesterol levels should
be measured at 6 and 12 weeks following introduction
of this diet. If the desired cholesterol level is not
achieved, drug therapy should be considered.

Triglycerides

The person with borderline hypertriglyceridemia
should be instructed to achieve and maintain ideal
body weight. Since weight reduction diets (caloricaUy-
controUed) are usually low in fat and high in carbo-
hydrate and this may increase serum triglyceride lev-
els, the National Cholesterol Education Program rec-
ommends that the fat content not be lowered beyond
the Step 1 diet.

Children

The current recommendations for children over two
years of age were published by the American Heart
Association.^ Presently, guidelines are being devel-
oped by a National Heart, Lung, and Blood Institute
Panel as part of the National Cholesterol Education
Program.

Resources

Educational materials are available from the National
Cholesterol Education Program and from the Amer-
ican Heart Association. The Louisiana affiliate of the
American Heart Association maintains patient edu-
cation materials in its office. ■

REFERENCES

1. Report of the expert panel on detection, evaluation, and treatment of high
blood cholesterol in adults. National Heart, Lung, and Blood Institute.
Arch Intern Med 1988;148:36.

JOURNAL VOL 140 MAY 45

2. Moore MC, Guzman MA, Schilling PE, et al: Dietary-artherosderosis study

on deceased persons. / Am Diet Assoc 1977;70:602.

3. Balart L, Moore MC, Gremillion L, et al: Serum lipids, dietary intakes

and physical exercise in medical students. / Am Diet Assoc 1974;64:42.

4. Dayton S, Pearce ML, Hashimota S, et al: A controlled clinical trial of a

diet high in unsaturated fat in preventing complications of atheroscle-
rosis. Circulation 1969;39-40(suppl 2).

5. Mattson FH, Grundy SM: Comparison of effect of dietary saturated, mon-

ounsaturated, and polyunsaturated fatty acids of lipids and lipoproteins
in man. } Lipid Red 1985;26:194.

6. Hegsted DM: Serum cholesterol response to dietary cholesterol: A re-

evaluation. Am J Clin Nutr 1986;44:299.

7. Kesardemi YA, Grundy SM: Increased low density lipoprotein production

associated with obesity. Artery 1983;3:170.

8. Schucker B, Bailey K, Heimbach JT, et al: Change in public perspective

on cholesterol and heart disease. JAMA 1987;258(24):3527.

9. Weidman W, Kwiterovich P, Jesse MJ, et al: Diet in the healthy child.

AHA Committee Report. Circulation 1983;67:1411A.

10. Connor WF, Cormor SL: Dietary treatment of hyperlipidemia, in Hyper-
lipidemia, Rifkind B, Levy R (eds). New York, Grune & Stratton, 1977:
p 297.

Ms Legardeur is an assistant professor of clinical medicine from the
Dept of Medicine, Nutrition Section, at LSU School of Medicine in

New Orleans.

Dr Lopez-S is a professor of medicine in the Dept of Medicine,
Nutrition Section, at LSU School of Medicine in New Orleans.

Reprints will not be available.

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46 JOURNAL VOL 140 MAY

PHARMACOLOGIC TREATMENT OF
HYPERCHOLESTEROLEMIA

STEVEN N. LEVINE, MD

Pharmacologic therapy for hypercholesterolemia is
indicated for those individuals with significant
elevations of the serum cholesterol following an
adequate trial of dietary modification. Initiation of
drug therapy is recommended for patients without
a history of coronary heart disease or other risk
factors if low density lipoprotein (LDL)-cholesterol
levels are ^ 190 mg/dl following at least six
months of adherence to a cholesterol lowering diet.
An LDL-cholesterol value of ^ 160 mg/dl is used
as a cutoff for those patients with coronary heart
disease or coronary risk factors. This article
provides information on the current drugs
available to manage patients with
hypercholesterolemia, including lovastatin, an
agent recently approved for clinical use. For each
drug a summary of the indicatioins, expected
response, potential side effects, and recommended

dosage is provided.

E pidemiological data, supported by animal and
genetic investigations, provide conclusive evi-
dence for a causal relationship between serum cho-
lesterol levels and the incidence of coronary heart
diseased Furthermore, clinical trials such as the Lipid
Research Clinic-Coronary Primary Prevention Trial
demonstrate that lowering of serum cholesterol levels
reduces the frequency of fatal and nonfatal myocar-
dial infarctions d Therefore, few would disagree with
recommendations to reduce cholesterol levels in
Western populations as a whole, and to specifically
lower cholesterol levels in patients with significant
elevations of total and low density lipoprotein (LDL)-
cholesterol.

This review focuses on the pharmacologic man-
agement of primary hypercholesterolemia. Other ar-
ticles in this issue deal with the evaluation and dietary
therapy of this group of disorders. However, several
points deserve emphasis. First, other etiologies of hy-
percholesterolemia, such as hypothyroidism must be
excluded before identifying and treating an individual
for primary hypercholesterolemia. Obviously, such
patients are treated in quite a different manner than
those with primary disorders of cholesterol metabo-
lism. Second, most individuals with hypercholester-
olemia can effectively be managed with dietary mod-

JOURNAL VOL 140 MAY 47

TABLE

RECOMMENDED LDL-CHOLESTEROL LEVELS FOR
INITIATING DRUG THERAPY FOLLOWING AN ADEQUATE
TRIAL OF DIET

LDL-cholesterol > 1 90 mg/dl — without definite CHD or two other
CHD risk factors

LDL-cholesterol > 1 60 mg/dl — with a history of definite CHD or
two other CHD risk factors.

CHD risk factors
Male sex

Family history of premature CHD
Cigarette smoking
Hypertension

Low HDL-cholesterol (< 35 mg/dl)

Diabetes mellitus

History of cerebrovascular or peripheral vascular disease
Severe obesity (> 30% overweight)

CHD = coronary heart disease

ifications, avoiding the need for long-term drug
administration. Third, hypercholesterolemia repre-
sents only one of several identified risk factors for
coronary heart disease. While treating the elevated
cholesterol, patients need to be counseled to reduce
other risk factors, such as smoking.

The recently released report from the National
Cholesterol Education Program provides specific rec-
ommendations and guidelines for initiating dietary
and pharmacologic therapy for hypercholesterol-
emia.^ Addition of drugs is recommended for those
patients who, following a minimum of six months of
strict dietary treatment, have persistent elevations of
LDL-cholesterol. The goal of therapy is to maximally
reduce LDL-cholesterol levels with agents such as bile
salt sequestrants and nicotinic acid. Recently, ap-
proval by the Food and Drug Administration of lo-
vastatin, an inhibitor of cholesterol synthesis, has pro-
vided clinicians with a new class of drug to reduce
serum cholesterol concentrations. Pharmacologic in-
tervention to raise high density lipoprotein (HDL)-
cholesterol levels represents an additional approach
to reducing coronary heart disease. A recent report
from the Helsinki Heart Stud)^ demonstrated a re-
duced rate of cardiac events in hyperlipidemic males
treated with gemfibrozil, an agent principally utilized
to lower triglyceride levels, but having the added ben-
efit of raising HDL-cholesterol concentrations.

For those individuals without a history of coro-

nary heart disease or two other coronary heart disease
risk factors, drug therapy is recommended if LDL-
cholesterol levels equal or exceed 190 mg/dl following
at least six months of adherence to a cholesterol low-
ering diet. An LDL-cholesterol value of ^ 160 mg/dl
is used as a cutoff for those patients with definite
coronary heart disease or two risk factors (Table). ^ The
goal of drug therapy is reduction of LDL-cholesterol
to < 160 mg/dl for those without coronary heart dis-
ease or risk factors and < 130 mg/dl for patients with
a history of, or at greater risk for, coronary heart dis-
ease.

BILE SALT SEQUESTRANTS

The bile salt sequestrants cholestyramine and coles-
tipol are considered first line drugs for management
of hypercholesterolemia.^ They have clearly been
demonstrated to reduce LDL-cholesterol levels, while
having minimal systemic toxicity since they are not
absorbed from the gastrointestinal tract. Both drugs,
being anionic binding resins, bind bile salts, reducing
their resorption from the terminal ileum, interrupting
the enterohepatic circulation. ^ The resulting reduc-
tion in the size of the bile salt pool stimulates hepatic
conversion of cholesterol to bile acids, increasing the
liver's demand for cholesterol. As a consequence, he-
patic synthesis of cholesterol increases, as does
expression of high affinity LDL receptors on the cell
surface.^ Increased cholesterol clearance via hepatic
LDL receptors is partially offset by increased hepatic
cholesterol synthesis, but the net effect is a 15% to
30% reduction in circulating LDL-cholesterol levels.
Concomitant administration of an hydroxymethyl-
glutaryl (HMG) CoA reductase inhibitor such as lo-
vastatin, significantly reduces the compensatory in-
crease in hepatic cholesterol synthesis, potentiating
the hypocholesterolemic effect of the bile salts se-
questrants.

Administration of bile salt sequestrants lowers
cholesterol in patients with a variety of etiologies of
primary hypercholesterolemia, including heterozy-
gotes for familial hypercholesterolemia. These indi-
viduals express only 50% of the normal quantity of
functional LDL receptors on cell membranes. The
administration of drugs that increase the number of
LDL receptors partially corrects the underlying path-
ophysiologic defect.^ Unfortunately these drugs (as
well as HMG CoA reductase inhibitors) provide no
beneficial effect in homozygotes for familial hyper-

48 JOURNAL VOL 140 MAY

cholesterolemia who lack the ability to express any
functional LDL receptors.

Cholestyrarnine is available in packets (5 g of drug
+ 4 g of flavored filler) or bulk containers. Similarly,
colestipol can be purchased in 5 g packets or bulk.
Both are granular powders that must be mixed with
water, juice, carbonated beverages, or foods such as
applesauce. As noted above, the bile salt sequestrants
are not absorbed from the gastrointestinal tract and
thus systemic toxicity is minimal. However, gastroin-
testinal complaints including constipation, bloating,
nausea, and flatulence are common. Constipation can
usually be managed by increasing dietary fiber or ad-
dition of a bulk laxative. Caution must be exercised
in administering bile salt sequestrants with other
medications, as the resins may bind a variety of drugs
including thyroxine, digitalis compounds, thiazide di-
uretics, phenylbutazone, beta blockers, phenobarbi-
tal, and warfarin. It is therefore advisable to admin-
ister other medications at least one hour before, or
four hours following, cholestyramine or colestipol.^' ^
Furthermore, large doses, particularly in patients with
hepatic or small bowel disease, may result in de-
creased absorption of fat soluble vitamins. However,
routine administration of vitamins is usually not nec-
essary in adults. The bile salt sequestrants tend to
cause modest elevations in serum triglyceride and are
best avoided as single agents in hypercholesterolemic
patients with concomitant triglyceride levels > 500
mg/dl.^

Most
patients
need
only one.

NICOTINIC ACID

Nicotinic acid has long been recognized as a hypo-
lipidemic agent whose primary action is to reduce
hepatic very low density lipoprotein (VLDL) synthe-
sis. Because VLDL serve as precursors for LDL pro-
duction, the serum concentrations of both lipopro-
teins decrease when pharmacologic doses of nicotinic
acid are administered.^ LDL-cholesterol typically de-
creases 15% to 25%, often accompanied by an increase
in HDL-cholesterol. This drug is considered a first line
agent for managing patients with hypercholestero-
lemia and generally considered the drug of choice for
patients with familial combined hyperlipidemia.^
Nicotinic acid, while quite efficacious, must be
administered cautiously due to its wide spectrum of
toxic effects. Prostaglandin-mediated cutaneous
flushing is a common complaint that can be reduced
by pretreatment with aspirin or other nonsteroidal ►

K-»UR20

(potassium chloride) 20mEq

Microburst

Release

System"

Sustained Release
Tablets

A daily prophylactic dose
in a single tablet.

Please see next page for brief summary of prescribing information.

Pharmaceuticals, Inc.
Kenilworth, NJ 07033

World leader in drug delivery systems.

K-9UK

(potassium chloride)

Microburst

Release

System"

Sustaned Release Tablets

INDICATIONS AND USAGE: BECAUSE OF REPORTS OF INTESTINAL AND GASTRIC ULCERATION AND
BLEEDING WITH SLOW-RELEASE POTASSIUM CHLORIDE PREPARATIONS, THESE DRUGS SHOULD
BE RESERVED FOR THOSE PATIENTS WHO CANNOT TOLERATE OR REFUSE TO TAKE LIQUID OR EF-
FERVESCENT POTASSIUM PREPARATIONS OR FOR PATIENTS IN WHOM THERE IS A PROBLEM OF
COMPLIANCE WITH THESE PREPARATIONS.

1. For therapeutic use In patients with hypokalemia with or without metabolic alkalosis, in digitaiis
intoxication and in patients with hypokalemic familial periodic paralysis.

2. For the prevention of potassium depletion when the dietary intake is inadequate in the following
conditions: Patients receiving digitalis and diuretics for congestive heart failure, hepatic cirrhosis
with ascites, states of aldosterone excess with normal renal function, potassium-losing nephropathy,
and with certain diarrheai states.

3. The use of potassium salts in patients receiving diuretics for uncomplicated essential hyperten-
sion is often unnecessary when such patients have a normal dietary pattern. Serum potassium
should be checked periodically, however, and if hypokalemia occurs, dietary supplementation with
potassium-containing foods may be adequate to control milder cases. In more severe cases sup-
plementation with potassium salts may be indicated.

CONTRAINDICATIONS: Potassium supplements are contraindicated in patients with hyperkalemia
since a further increase in serum potassium concentration in such patients can produce cardiac
arrest. Hyperkalemia may complicate any of the following conditions: Chronic renal failure, systemic
acidosis such as diabetic acidosis, acute dehydration, extensive tissue breakdown as in severe burns,
adrenal insufficiency, or the administration of a potassium-sparing diuretic (e.g., spironolactone,
triamterene).

Wax-matrix potassium chloride preparations have produced esophageal ulceration in certain cardi-
ac patients with esophageal compression due to enlarged left atrium.

All solid dosage forms of potassium chloride supplements are contraindicated in any patient in
whom there is cause for arrest or delay in tablet passage through the gastrointestinal tract. In these
instances, potassium supplementation should be with a liquid preparation.

WARNINGS: Hyperkalemia— In patients with impaired mechanisms for excreting potassium, the ad-
ministration of potassium salts can produce hyperkalemia and cardiac arrest. This occurs most com-
monly in patients given potassium by the intravenous route but may also occur in patients given
potassium orally. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of
potassium salts in patients with chronic renal disease, or any other condition which impairs potas-
sium excretion, requires particularly careful monitoring of the serum potassium concentration and
appropriate dosage adjustment.

Interaction with Potassium Sparing Diuretics— Hypokalemia should not be treated by the con-
comitant administration of potassium salts and a potassium-sparing diuretic (e.g., spironolactone or
triamterene) since the simultaneous administration of these agents can produce severe hyperkalemia.

Gastrointestinal Lesions— Potassium chloride tablets have produced stenotic and/or ulcerative
lesions of the small bowel and deaths. These lesions are caused by a high localized concentration of
potassium ion in the region of a rapidly dissolving tablet, which injures the bowel wall and thereby
produces obstruction, hemorrhage or perforation.

K-DUR tablets contain micro-crystalloids which disperse upon disintegration of the tablet. These
micro-crystalloids are formulated to provide a controlled release of potassium chloride. The dispersi-
bility of the micro-crystalloids and the controlled release of ions from them are intended to minimize
the possibility of a high local concentration near the.gastrointestinal mucosa and the ability of the KOI
to cause stenosis or ulceration. Other means of accomplishing this (e.g., incorporation of potassium
chloride into a wax matrix) have reduced the frequency of such lesions to less than one per 100,000
patient years (compared to 40-50 per 100,000 patient years with enteric-coated potassium chloride)
but have not eliminated them. The frequency of Gl lesions with K-DUR tablets is, at present,
unknown. K-DUR tablets should be discontinued immediately and the possibility of bowel obstruction
or perforation considered if severe vomiting, abdominal pain, distention, or gastrointestinal bleeding
occurs.

Metabolic Acidosis— Hypokalemia in patients with metabolic acidosis should be treated with an
alkalinizing potassium salt such as potassium bicarbonate, potassium citrate, potassium acetate, or
potassium gluconate.

PRECAUTIONS: The diagnosis of potassium depletion is ordinarily made by demonstrating hypokale-
mia in a patient with a clinical history suggesting some cause for potassium depletion. In interpreting
the serum potassium level, the physician should bear in mind that acute alkalosis per se can produce
hypokalemia in the absence of a deficit in total body potassium while acute acidosis per se can in-
crease the serum potassium cohcentration into the normal range even in the presence of a reduced
total body potassium. The treatment of potassium depletion, particularly in the presence of cardiac
disease, renal disease, or acidosis requires careful attention to acid-base balance and appropriate
monitoring of serum electrolytes, the electrocardiogram, and the clinical status of the patient.

Laboratory Tests: Regular serum potassium determinations are recommended. In addition, during
the treatment of potassium depletion, careful attention should be paid to acid-base balance, other
serum electrolyte levels, the electrocardiogram, and the clinical status of the patient, particularly in
the presence of cardiac disease, renal disease, or acidosis.

Drug Interactions: Potassium-sparing diuretics; see WARNINGS.

Carcinogenesis, Mutagenesis, Impairment of Fertility: Long-term carcinogenicity studies in
animals have not been performed.

Pregnancy Category C: Animal reproduction studies have not been conducted with K-DUR. It is
also not known whether K-DUR can cause fetal harm when administered to a pregnant wqman or can
affect reproduction capacity, K-DUR should be given to a pregnant woman only if clearly needed.

Nursing Mothers: The normal potassium ion content of human milk is about 13 mEq per liter. Since
oral potassium becomes part of the body potassium pool, so long as body potassium is not exces-
sive, the contribution of potassium chloride supplementation should have little or no effect on the
level in human milk.

Pediatric Use: Safety and effectiveness in children have not been established.

ADVERSE REACTIONS: One of the most severe adverse effects is hyperkalemia (see CONTRAINDICATIONS,
WARNINGS, and OVERDOSAGE). There have also been reports of upper and lower gastrointestinal
conditions including obstruction, bleeding, ulceration, and perforation (see CONTRAINDICATIONS
and WARNINGS): other factors known to be associated with such conditions were present in many of
these patients.

The most common adverse reactions to oral potassium salts are nausea, vomiting, abdominal dis-
comfort, and diarrhea. These symptoms are due to irritation of the gastrointestinal tract and are best
managed by taking the dose with meals or reducing the dose.

Skin rash has been reported rarely.

OVERDOSAGE: The administration of oral potassium salts to persons with normal excretory mecha-
nisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are im-
paired or if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can
result (see CONTRAINDICATIONS and WARNINGS), It is important to recognize that hyperkalemia is
usually asymptomatic and may be manifested only by an increased serum potassium concentration
and characteristic electrocardiographic changes (peaking of T-waves, loss of P-waves, depression of
S-T segment, and prolongation of the QT-interval). Late manifestations include muscle-paralysis and
cardiovascular collapse from cardiac arrest.

Treatment measures for hyperkalemia include the following:

1. Elimination of foods and medications containing potassium and of potassium-sparing diuretics.

2. Intravenous administration of 300 to 500 ml/hr of 10% dextrose solution containing 10-20 units
of insulin per 1,000 ml.

3. Correction of acidosis, if present, with intravenous sodium bicarbonate.

4. Use of exchange resins, hemodialysis, or peritoneal dialysis.

In treating hyperkalemia, it should be recalled that in patients who have been stabilized on
digitalis, too rapid a lowering of the serum potassium concentration can produce digitalis toxicity.

1002004

##"■# Key Pharmaceuticals, Inc.

Kenilworth, NJ 07033 (USA)

World leader in drug delivery systems.

13944326
Rev. 4/87

anti-inflammatory agents. Tolerance to this side effect
usually develops and symptoms can be limited by
slowly titrating the dose of nicotinic acid upward.
However, if doses are omitted the flushing tends to
worsen, and thus education concerning proper •
administration is essential if patient compliance is ex- ■
pected. Abdominal discomfort, diarrhea, as well as
flushing, can be limited by administering the drug
with food. Additional side effects include hepatic dys-
hmction, hyperuricemia, glucose intolerance, dry skin,
increased skin pigmentation with acanthosis nigri-
cans, cardiac arrhythmias, and activation of peptic
ulcer disease. Nicotinic acid is contraindicated in pa- I
tients with hepatic disease, gout, significant hyper-
uricemia, peptic ulcer disease, or significant cardiac ,
arrhythmias, and should be used with caution in pa- j
tients with diabetes mellitus. Liver function tests, glu- , i
cose, and uric acid should be monitored periodically ! ;
in patients treated with this drug. !

Nicotinic acid therapy is initiated at a low dose, ‘ j
100 mg one to three times/day with meals. The dose |
is slowly titrated upward every four to seven days,
depending on individual tolerance to side effects, par-
ticularly flushing. Since toxic reactions to nicotinic
acid tend to occur at higher doses, it is recommended
that the therapeutic response be measured once the
dose has reached 2 g per day. If a satisfactory lowering
of LDL-cholesterol has not been achieved at this lower

dose, an increase to 3 g per day is recommended. j
Further increases up to 6 g per day are occasionally ;
necessary to achieve the desired response. ^

Nicotinic acid has proved to be particularly ef-
fective in lowering cholesterol when used in combi-
nation with cholestyramine or colestipol. Patients with
significant hypercholesterolemia able to tolerate full
therapeutic doses of both drugs can commonly achieve
normal LDL-cholesterol levels.®

HMG CoA REDUCTASE INHIBITORS

The discovery of fungal metabolites that competitively
inhibit HMG CoA reductase, the rate limiting enzyme
in cholesterol synthesis, provides clinicians with a
new class of pharmacologic agent to manage hyper-
cholesterolemia. Lovastatin (formerly referred to as
mevinolin) is the first such agent approved for use by
the Food and Drug Administration. Increased syn-
thesis of HMG CoA reductase partially compensates
for reduced hepatic cholesterol synthesis. However,
reduced cholesterol synthesis causes increased num-

bers of LDL-receptors on hepatic membranes, low-
ering LDL levels by increasing receptor-mediated ca-
tabolism of this lipoprotein/ Additional data suggests
that lovastatin also results in a modest decrease in
LDL production.

Used as a single agent, lovastatin typically lowers
total cholesterol levels by 20% to 35%, LDL-choles-
terol levels by 25% to 45%, and increases HDL-cho-
lesterol concentrations 6% to 10% in individuals with
both nonfamilial hypercholesterolemia and hetero-
zygotes for familial hypercholesterolemia.^' Com-
bined therapy with bile salt sequestrants and lova-
statin lowers cholesterol levels to a greater degree
than either agent alone. This combination of drugs is
particularly attractive since lovastatin blocks the com-
pensatory increase in cholesterol synthesis that occurs
when a bile salt sequestrant is used alone. ^ As a con-
sequence, an even greater number of LDL-receptors
are expressed, further increasing receptor-mediated
LDL uptake and catabolism (Fig 1). Combined ther-
apy can result in reductions of LDL-cholesterol of up
to 60%. Unfortunately, lovastatin is not beneficial in
the treatment of homozygotes for familial hypercho-
lesterolemia, since such patients cannot express any
functional LDL-receptors. An exception has been a
patient treated by liver transplantation (providing a
source of LDL-receptors) followed by lovastatin ther-
apy.7

Lovastatin is generally well-tolerated. Occasional
patients have reported abnormalities in bowel func-
tion, headaches, or pruritus that usually do not re-
quire discontinuation of therapy. Infrequently the drug
may cause myositis with increases in creatine phos-
phokinase (CPK), and rarely rhabdomyolysis. Pa-
tients on lovastatin must have liver function tests
monitored at frequent intervals (every four to six weeks
for 15 months) since up to 1.9% of treated patients
develop persistent elevations of transaminase levels
that require discontinuation of the drug. An addi-
tional concern is the possible association of lovastatin
with the development of lens opacifications. There-
fore, patients should have an initial and annual slit
lamp examination.^

Recommended doses are between 20 mg/day to
80 mg/day. Therapy is initiated at a dose of 20 mg
with the evening meal, although an initial dose of 20
mg twice a day may be chosen for patients with severe
hypercholesterolemia (cholesterol >300 mg/dl). The
maximal hypocholesterolemic response to a particular
dose is typically obtained by four weeks of therapy

and thus increases in dosage should not be made
more frequently than monthly. Patients do not de-
velop tolerance to the cholesterol-lowering effects of
lovastatin; the beneficial response persists as long as
the drug is continued.^- Since cholesterol serves as
a precursor for steroid hormone biosynthesis, phar-
macologic agents that inhibit cholesterol production
might potentially result in adrenal or gonadal steroid
hormone deficiencies. However, studies of endocrine
function in patients treated with lovastatin have failed
to demonstrate any evidence of such deficiencies.^^

Lovastatin, as well as newer analogs that are un-
der investigation, are potent hypocholesterolemic
agents representing a significant advance in the treat-
ment of hypercholesterolemia. However, enthusiasm
for their administration must be tempered until long-
term safety has been adequately determined.^

PROBUCOL

Probucol is a fat soluble compound that lowers serum
cholesterol concentrations by a mechanism that stiU
remains incompletely characterized. The drug in-
creases the fractional catabolic rate of LDL and may
increase clearance by a mechanism independent of
the high affinity LDL-receptor. A pharmacologic dose
of probucol typically lowers LDL-cholesterol concen-
trations 10% to 15% but at the same time has the
disturbing property of reducing HDL-cholesterol by
as much as 25%.^

The drug is usually weU tolerated with few side
effects. Diarrhea, abdominal pain, nausea, and flat-
ulence are occasionally noted, but often transient, not
requiring discontinuation of therapy. Probucol can
prolong the QT interval and is arrhythmogenic in ex-
perimental animals, although no increased frequency
of cardiac arrhythmias has been noted in humans.
However, it should be used with extreme caution, or
not at all, in patients with prolonged QT intervals or
clinical evidence of myocardial irritability.^

The usual dose is 500 mg twice a day. Due to its
lipid solubiLity, serum concentrations decrease slowly
following discontinuation of therapy. Concern over
the reduction in HDL-cholesterol levels produced by
probucol has generally led physicians to restrict its
use to hypercholesterolemic patients who are intol-
erant of other modalities of therapy.

CLOFIBRATE

Clofibrate, a fibric acid derivative, is a hypolipidemic ►

JOURNAL VOL 140 MAY 51

agent mainly used to lower serum triglyceride levels
in patients at risk for developing pancreatitis. Its prin-
cipal action is to enhance removal of triglyceride-rich
lipoproteins by increasing the activity of lipoprotein
lipase.^ LDL-cholesterol levels are only slightly re-
duced, Clofibrate increases biliary excretion of neutral
sterols, increasing the lithogenicity of bile and the
incidence of cholelithiasis. Other side effects include
nausea, abdominal discomfort, decreased libido, and
transient abnormalities in liver function. Myositis as-
sociated with increased levels of CPK may occur, par-
ticularly in patients with renal insufficiency. The drug
also potentiates the action of coumadin and should
be used with caution in patients receiving oral anti-
coagulants. A concern of long-term safety was raised
by a World Health Organization study in which pa-
tients treated with clofibrate experienced an increased
incidence of noncardiac deaths mainly due to a greater
number of malignancies.^

The usual dose of clofibrate is 1 g twice daily. It
is particularly efficacious in the management of pa-
tients with dysbetalipoproteinemia who have ele-
vated concentrations of beta-VLDL, It is also benefi-
cial for treatment of patients with significant elevations
of serum triglyceride at risk for developing pancrea-
titis, but has a very limited role for use in patients
with elevated concentrations of LDL-cholesterol.

GEMFIBROZIL

The principal use of gemfibrozil, another fibric acid
derivative similar in structure to clofibrate, is to lower
the triglyceride concentration. The drug has variable
effects on LDL-cholesterol, but can reduce its con-
centration in patients without significant hypertri-
glyceridemia. Gemfibrozil has the added benefit of
raising HDL-cholesterol concentrations by 10% to
15%.^ The drug, like clofibrate, increases lipoprotein
lipase activity but has an additional effect of reducing
VLDL synthesis. The spectrum of side effects is sim-
ilar to clofibrate, although gemfibrozil seems less Ukely
to cause cholelithiasis.^

The recent publication of the Helsinki Heart Study
provided evidence that administration of gemfibrozil
to patients with elevated non HDL-cholesterol levels
can reduce the incidence of coronary heart disease.^
Compared to placebo treated subjects, those receiving
gemfibrozil (600 mg twice daily for five years) had a
7% to 9% decrease in total cholesterol, 8% to 9% de-
crease in LDL-cholesterol, 30% to 40% decrease in

triglyceride, and 8% to 10% increase in HDL-choles-
terol. Treated patients had a 34% reduction in coro-
nary heart disease end points (fatal or nonfatal my-
ocardial infarction and cardiac death). A modest
increase in gastrointestinal symptoms occurred in the
gemfibrozil treated group, however, no significant in-
crease in malignancies was apparent during the five
years of the study. The mechanism responsible for
the reduced incidence of coronary heart disease in the
Helsinki study is difficult to define since patients with
variable lipoprotein patterns participated and poten-
tially beneficial changes in several of the lipoprotein
fractions were observed. However, it is likely that the
increase in HDL-cholesterol played a major role in
reducing the incidence of cardiac events.

NEOMYCIN

Neomycin is considered a second line agent for the
treatment of hypercholesterolemia in patients unable
to tolerate more standard therapy.^ It is a poorly ab-
sorbed antibiotic that lowers LDL-cholesterol levels
by inhibiting the intestinal absorption of cholesterol.
Typically serum LDL-cholesterol levels decrease 15%
to 25%. Like other aminoglycoside antibiotics, neo-
mycin has the potential to cause nephrotoxicity and
ototoxicity. However, these complications are rela-
tively uncommon if neomycin is not prescribed for
patients with renal impairment or those with gas-
trointestinal diseases that might allow for increased
absorption of the drug.^ More commonly, patients
may experience abdominal cramps or diarrhea. The
usual dose is one g twice a day. Hoeg et al reported
that a regimen of neomycin in combination with nic-
otinic acid was able to lower LDL-cholesterol levels
by 45% in those patients able to tolerate the prescribed
doses of both drugs.

DEXTROTHYROXINE

Dextrothyroxine, the optical isomer of 1-thyroxine,
can lower LDL-cholesterol concentrations by 10% to |
20%. The drug increases LDL catabolism by stimu-
lating activity of hepatic high affinity LDL-receptors.
However, the hypocholesterolemic effect of dextro-
thyroxine is achieved at the expense of producing a
mild state of thyrotoxicosis.^ Effective doses may ex-
acerbate angina, and cause nervousness, tremor,
sweating, and cardiac arrhythmias. Bantle et al dem-
onstrated that equivalent doses of d- and 1-thyroxine

52 JOURNAL VOL 140 MAY

Fig. Complementary action of combined therapy
with a bile salt sequestrant plus an inhibitor
of HMG CoA reductase in the treatment of hy-
percholesterolemia (© Nobel Foundation,
1986 ).

(based on suppression of the thyroid-stimulating hor-
mone response to thyrotropin releasing hormone)
produced comparable decreases in LDL-cholesterol
levels. D-thyroxine is usually initiated at a dose of
2 mg per day. The dose is titrated up by 1 mg incre-
ments to a maximal dose of 4 mg to 6 mg per day.
The drug should not be used in patients with evidence
of cardiac disease or older individuals who might have
asymptomatic coronary stenoses.^' ^ Due to its effect
on accelerating metabolism and its potential to ex-
acerbate coronary heart disease, dextrothyroxine has
a very limited place in the management of hypercho-
lesterolemia.

COMBINATION THERAPY

For those individuals with hypercholesterolemia who
do not achieve a satisfactory lowering of the serum
cholesterol on single drug therapy, a combination of
drugs may enhance the therapeutic response. Patients
who are heterozygotes for familial hypercholester-
olemia typically need treatment with more than a sin-
gle agent in order to normalize cholesterol levels. Pref-
erably, agents are chosen that lower cholesterol levels
by different mechanisms of action. ^ Bile salt seques-
trants together with nicotinic acid have been used
successfully for many years. This combination is par-
ticularly helpful to lower triglyceride levels in patients
who develop elevations of this lipid on sequestrants
alone. When used together total cholesterol levels de-
crease by 45% and LDL-cholesterol by 55%. ® More
recently, the addition of lovastatin to a bile salt se-
questrant has proved extremely successful as a hy-
pocholesterolemic regimen. Lovastatin, by blocking
the enhanced cholesterol synthesis that occurs when

cholestyramine or colestipol is used alone, enhances
the increase in hepatic LDL-receptors and augments
the therapeutic response (Fig).^ Typically, a decrease
of 55% can be achieved in LDL-cholesterol in patients
with nonfamilial hypercholesterolemia and hetero-
zygotes for familial hypercholesterolemia.^^' Many
other combinations of hypocholesterolemic agents
have been used in limited numbers of patients. Gen-
eral recommendations must await additional studies
evaluating the efficacy and side effects of such com-
binations. ■

ACKNOWLEDGMENTS

Thanks to Drs Brown and Goldstein and the Nobel
Foundation for permission to reprint the figure.

REFERENCES

1. Grundy SM: Cholesterol and coronary heart disease; A new era. JAMA
1986;256:2849-2858.

2. Lipid Research Clinics Program. The lipid research clinics coronary pri-
mary prevention trial results: I Reduction in incidence of coronary heart
disease. JAMA 1984;251:351-364.

3. The Expert Panel: Report of the National Cholesterol Education Program
expert panel on detection, evaluation, and treatment of high blood cho-
lesterol in adults. Arch Intern Med 1988;148:36-69.

4. Frick MH, Elo O, Haapa K, et al: Helsinki Heart Study: Primary-pre-
vention trial with gemfibrozil in middle-age men with dyslipidemia:
Safety of treatment, changes in risk factors, and incidence of coronary
heart disease. N Engl J Med 1987;317:1237-1245.

5. Brown WV, Goldberg IJ, Ginsberg HN: Treatment of common lipopro-
tein disorders. Prog Cardiovasc Dis 1984;27:1-20.

6. Illingworth DR: Lipid-lowering drugs: An overview of indications and
optimum therapeutic use. Drugs 1987;33:259-279.

7. Brown MS, Goldstein JL: A receptor-mediated pathway for cholesterol
homeostasis. Science 1986;232:34-47.

8. Kane JP, Malloy MJ, Tun P, et al: Normalization of low-density-Upopro-
tein levels in heterozygous familial hypercholesterolemia with a com-
bined drug regimen. N Engl J Med 1981;304:251-258.

9. Lovastatin Study Group II: Therapeutic response to lovastatin (mevi-
nolin) in nonfamilial hypercholesterolemia: A multicenter study. JAMA
1986;256:2829-2834.

10. Havel RJ, Hunninghake DB, lUingworth R, et al: Lovastatin (mevinolin)
in the treatment of heterozygous familial hypercholesterolemia. Ann In-
tern Med 1987;107:609-615.

11. Farnsworth WH, Hoeg JM, Brittain EH, et al: Testicular function in type
II hyperlipoproteinemic patients treated with lovastatin (mevinolin) or
neomycin. J Clin Endocrinol Metab 1987;65:546-550.

12. Hoeg JM, Maher MB, Bou E, et al: Normalization of plasma lipoprotein
concentrations in patients with type II hyperlipoproteinemia by com-
bined use of neomycin and niacin. Circulation 1984;70:1004-1011.

13. Bantle JP, Hunninghake DB, Frantz ID, et al; Comparison of effectiveness
of thyrotropin-suppressive doses of d- and 1-thyroxine in treatment of
hypercholesterolemia. Am J Med 1984;77:475-481.

14. Vega LG, Grundy SM: Treatment of primary moderate h 5 ^ercholester-
olemia with lovastatin (mevinolin) and colestipol. JAMA 1987;257:33-38.

15. Illingworth DR: Mevinolin plus colestipol in therapy for severe hetero-
zygous famiHal hypercholesterolemia. Ann Intern Med 1984;101:598-604.

Dr. Levine is with the Dept of Medicine, Section of Endocrinology, at

LSU Medical Center in Shreveport.

Reprint requests should be sent to Steven N. Levine, MD, LSU Medical
Center, Dept of Medicine, Section of Endocrinology, PO Box 33932,

Shreveport, LA 71130.

JOURNAL VOL 140 MAY 55

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Heart transplantation: The Louisiana experience

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JOURNAL

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"" OF THE LOUISIANA STATE MEDICAL SOCIETY

1988

VOLUME 140 / NUMBER 6 /

JUNE

ARTICLES

John L. Ochsner, MD

Heart transplantation:

Clement C. Eiswirth Jr, MD

The Louisiana experience

Mary Lyn T. Lu, MD

Microsurgery in breast

William M. Swartz, MD

reconstruction using the
superior gluteus for free
tissue transfer: A case report

Neil Baum, MD

Surgical management of
impotence: New modalities

DEPARTMENTS

Information for Authors

ECG of the Month

Otolaryngology/Head

& Neck Surgery Report

Book Reviews

Books Received

Auxiliary Report

Calendar

Classified Advertising

Cover illustration by Barbara Seide, New Orleans

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ECG OF THE MONTH

THE COLD FACTS

JORGE I. MARTINEZ-LOPEZ, MD

The 12-lead tracing shown left
belongs to a 19-year-old man.
It was recorded several days
after a traumatic fracture of
his fifth cervical spine with
posterior displacement. Med-
ications included dexameth-
asone and cimetidine.

What is your diagnosis?
Elucidation is on page 5.

JOURNAL VOL 140 JUNE 3

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ECG of the Month

Case presentation is on page 3.

DIAGNOSIS — Spontaneous hypothermia

Profound sinus bradycardia with sinus arrhythmia,
at rates from 33 to 42 a minute, is present. The PR
interval is normal. QRS complexes appear broad and
display an upward notch in the downstroke of the
QRS in leads 1,2,3, AVF, and V2 through V6; AVR
shows a notch directed downward. Elevated ST seg-
ments with a concavity downward are recorded in
leads 1,2, AVR, and V2 through V6. Upright T waves
are found in all leads except AVR and display a ter-
minal notch in V3. Lastly, the QT interval is length-
ened to 0.56 second.

This constellation of ECG findings is consistent
with the clinical diagnosis of hypothermia and is the
subject of the discussion to follow.

DISCUSSION

Hypothermia — as measured with a low-reading rec-
tal thermometer — is defined as central body tem-
perature (core body temperature) of 34° C or lower.
This condition may develop as a result of either ac-
cidental or iatrogenic exposure to low environmental
temperatures and, less frequently, it is secondary to
acute medical or surgical disorders that are unrelated
to exposure (spontaneous). In this last group, hy-
pothermia often goes unrecognized because conven-
tional rectal thermometers do not record temperatures
lower than 35° C. Hypothermia may occur in the pres-
ence or absence of cardiac disease.

The patient whose tracing is shown here was
found to be hypothermic at the time the 12-lead ECG
was recorded. However, the exact core body tem-
perature was not established because of the unavail-
ability of the proper type of rectal thermometer. The
abnormal ECG findings were ascribed to hypother-
mia.

The characteristic ECG features found in hypoth-
ermia are predictable and reproducible experimen-
tally, appear sequentially as body temperature drops
below normal, and disappear gradually with rewarm-
ing. Cold core body temperatures depress cardiac au-
tomaticity. Consequently, the majority of hypoth-
ermic patients show sinus rates in the low 30s to the

high 40s. At extremely low core body temperatures,
some patients may develop atrial fibrillation, sino-
ventricular conduction or junctional escape rhythm.

The long QT interval found in hypothermia has
been attributed to increases in the duration of ven-
tricular repolarization as a result of myocardial cooling
and not to delayed ventricular depolarization.

One of the most important clues on the ECG of
the hypothermic patient is the extra deflection or notch
recorded at the QRS-ST junction. This deflection,
originally described by Tomaszewski in 1938, has been
given the eponymic designation of the Osborn wave.
Other terms applied to this deflection include: J de-
flection, J wave, camel hump wave, dromedary wave,
and hypothermic hump. The emergence of the Os-
born wave on the ECG is inversely related to the core
body temperature, but its mechanism of production
remains unclear. This wave may be overlooked if only
a single ECG lead is recorded or examined. The Os-
born wave is most commonly found in limb leads 2,3,
AVF, and precordial leads V5 and V6, and is directed
upward; when present in AVR and VI, it is directed
downward. As hypothermia deepens, the Osborn
wave tends to appear in all leads and become more
anteriorly oriented in the precordial leads. Although
the amplitude and duration of the Osborn wave di-
minish gradually with rewarming, in very few cases
it may persist for some time thereafter or perma-
nently.

As an isolated ECG finding, the Osborn wave is
not diagnostic of hypothermia. This wave has been
seen frequently in normothermic young adults who
have no demonstrable cardiac or extracardiac disease.

In patients with induced and accidental hypo-
thermia, fine oscillations of the baseline due to muscle
tremor artifacts are recorded often. These artifacts
make it difficult to identify atrial electrical activity and
to determine the cardiac rhythm. In such cases, di-
agnostic procedures that may be considered include
echocardiography and His bundle electrography. M-
mode echocardiography is helpful in identifying "A"
waves. In some patients, however, "A” waves were
recorded even though P waves were absent from the
ECG. Although His bundle electrography may be of
diagnostic utility, it is prudent not to use this invasive
procedure because hypothermic patients are already
critically Ul and experience a high mortality rate.

The electrical causes of death in hypothermic ►

JOURNAL VOL 140 JUNE 5

patients include ventricular fibrillation and cardiac
asystole. Most often, the terminal rhythm is cardiac
asystole.

There you have it. Those are . . . the cold facts!

SELECTED REFERENCES

1. Drake CE, Flowers NC: ECG changes in hypothermia from sepsis and
unrelated to exposure. Chest 1980;77:685-686.

2. Okada M, Nishimura F, Yoshino H, et al: The J wave in accidental hy-
pothermia. / Electrocardiol 1983;16:23-28.

3. del Bosco CG, Poderoso JJ, BiancoUni CA, et al: Hallazgos electrocardi-
ograficos en la hipotermia secondaria a enfermedades agudas. Medicim
1983;43:629-638.

4. Rankin AC: Cardiac arrhythmias during rewarming of pahents with ac-
cidental hypothermia. Brit Med J 1984;289:874-877.

5. Okada M: The cardiac rhythm in accidental hypothermia. J Electrocardiol
1984;17:123-128.

Dr. Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, Texas.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

Reprints will not be available.

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6 JOURNAL VOL 140 JUNE

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

CHRONIC HALITOSIS FROM
TONSILLOLITHS:

A COMMON

STEVEN M. FLETCHER, MD;

Chronic halitosis from tonsilloliths represents a
common^ yet oftentimes overlooked problem in
clinical otolaryngologic practice. A case of a 28-
year-old woman with this condition is presented
followed by a discussion of its pathophysiology
and management. The most common etiologies of
chronic halitosis are also indicated.

ETIOLOGY

PAUL A. BLAIR, MD, FACS

A 28-year-old woman gave a history of chronic in-
termittent halitosis which had been present for
several years and which had remained unresponsive
to long-term use of various mouth washes and per-
oxide rinses. As a child, she had suffered from mul-
tiple episodes of follicular tonsillitis which had re-
solved following medical therapy. On rare occasions
in her adult life, she had continued to have bouts,
the most recent of which having occurred several
months previously. She denied any history of upper
respiratory tract infections, nasal or paranasal sinus
disorders, smoking, dental or oral cavity disease, and
other known medical conditions. Family history
showed her mother had also suffered from chronic
halitosis for which she was treated by a tonsillectomy
for cryptic follicular tonsillitis with tonsilloliths with
complete resolution of her problem. Physical exami-
nation of the patient on admission was remarkable
only for moderately enlarged cryptic tonsils with nu-
merous small caseous plugs and multiple calcareous
particles protruding from the crypts of the tonsils. No
other demonstrable lesions of the upper aerodigestive

JOURNAL VOL 140 JUNE 7

tract were noted; adequate dental hygiene was ap-
parent. She subsequently underwent an elective ton-
sillectomy with an unremarkable postoperative re-
covery. The halitosis condition has been under
complete control under a follow-up period of one year.

Chronic halitosis is a distinctly unpleasant odor
to the breath. Etiology is due primarily to five groups
of conditions. Septic or putrefactive disease within
the oral cavity, nose, or paranasal sinuses is the group
most often causing halitosis. Chronic tonsillitis with
tonsilloliths constitutes one of the more common
members of this group. Stomatitis, gingivitis, glos-
sitis, periodontal disease, and carious teeth with en-
trapped fermenting food particles all reflect local de-
composition of the mouth from which the fetid odor
is generated. Nasal, pharyngeal, and sinus infectious
conditions (ie, suppurative rhinosinusitis, syphilis,
carcinoma of the upper aerodigestive tract, foreign
bodies [in children], chondronecrosis or osteonecrosis
of the nasal skeleton, allergic catarrh, atrophic rhinitis
and chronic pharyngitis) can all give rise to foulness
of the breath.

Perhaps the second most common etiology of hal-
itosis would be such ingested or inhaled substances
as onions, garlic, paraldehyde, tobacco smoke, alco-
hol, and certain drugs whose volatile products are
excreted at least in part by the lungs or salivary glands.

Putrefactive diseases of the lung may cause fetid
breath odor. The underlying thoracic pathology is
generally indicated by abundant putrid sputum, fre-
quent chest symptoms, and usually readily apparent
abnormal thoracic physical signs. Pyogenic, tuber-
culous, or other granulomatous diseases of the lung
presenting as bronchitis, gangrene, bronchiectasis,
empyema, or abscess may generate malodorous
breath.^

Severe alimentary tract or peritoneal disorders
may uncommonly cause halitosis. Foul breath usually
does not signify gastrointestinal disorders because the
esophagus is normally collapsed and anatomically
separate from the airway. Certain disease states such
as tracheoesophageal fistula, bronchoesophageal fis-
tula,^ or gastrointestinal disturbances associated with
severe gastroesophageal reflux may precipitate a com-
munication between the esophagus and the upper
respiratory tract. A disagreeable taste and odor may
emanate from this communication. Some systemic
diseases have characteristic odors: diabetic ketoaci-

dosis a fruity odor, hepatic failure a musty or fishy
odor, and azotemia a uriniferous odor.

Psychogenic causes namely the rumination syn-
drome or merycism and hypochondriacal states can
contribute to halitosis. Obsession with one's self-
cleanliness and paranoid delusions of self-destruction
of one's body organs have both been delineated as
the underlying disorder in many psychiatric patients
with halitosis.

Tonsilloliths are spiculated concretions of calcar-
eous or gritty particles which occur as a result of dep-
osition of inorganic salts in the debris that accumu-
lates within the crypts of tonsils in chronic follicular
tonsillitis. These calculi, which occur much more fre-
quently in adults than in children, are usually rounded
or oval particulate matter. They may vary in size from
multiple small stones within the substance of the ton-
sil or tonsillar crypts to a single large stone which may
be partially or completely embedded in the tonsil.^
Tonsilloliths represent the product of repeated in-
flammatory episodes of the tonsils which often re-
main clinically subacute. The cryptic openings on the
exterior of the tonsil often develop fibrosis with en-
trapment of squamous debris, particulate food matter,
and normal oral flora including bacterial, fungal, and
actinomyces-like organisms. The fermentation proc-
ess within this inflamed tonsillar pocket then gener-
ates the putrid odor and hence clinical halitosis.

Calculi of the tonsil must be differentiated from 1
other clinical entities, namely: calcified granulomas, !
foreign bodies (especially in children), malignant neo-
plasia of the tonsillar region, embryonic branchial arch
osseous or cartilaginous rests, or an elongated styloid
process protruding from the posterior aspect of the
tonsillar fossa. ^

Clinically most patients present as, in the case
report, with a history of multiple episodes of recurrent
acute tonsillitis in childhood and subsequently as
adults may complain of foreign body sensation, bad
taste in the mouth, nonspecific odynophagia, chronic ^
cough or gagging, or otalgia.

Physical examination usually reveals bilateral
cryptic tonsils which often contain caseous plugs of
debris or tonsilloliths with or without local inflam- j
mation. A careful search for the multiple other causes |
of halitosis especially of the oral, nasal, and sinus i
cavities is indicated to eliminate those conditions. Ex- !
elusion of periodontal or apical tooth infections or
food particle impactions, even in persons exercising

8 JOURNAL VOL 140 JUNE

regular tooth brushing and oral hygiene, is essential
in establishing the cryptic tonsil as the culprit.

The treatment of tonsilloliths and their associated
chronic tonsillitis, which may be subclinical, is re-
moval of the tonsillar calculi when possible, as with
a single stone or a limited number of larger stones or
tonsilloliths. Temporizing measures of frequent mouth
rinses or peroxide gargles following all meals and
snacks can achieve sufficient control of halitosis in
some patients but requires habitual long term daily
usage. The definitive removal of the nidus of this
condition, by tonsillectomy, remains the most satis-
factory permanent solution to this problem.

In summary, tonsilloliths with their associated
! chronic follicular tonsillitis represent one of the more
common, yet oftentimes overlooked, causes of chronic
halitosis in adults. The various common etiologies of
, halitosis are presented with control of the condition
' obviously resting upon control of the underlying dis-
1 ease process. Following elimination of other common
4 causes of halitosis, especially those arising from the
I oral cavity, low-grade, often subclinical, cryptic ton-
i sillitis with calculi and caseous debris should be con-
1 sidered as the cause of malodorous breath. When es-
tablished as the underlying cause of halitosis,
tonsilloliths may be definitively treated to achieve
( lasting resolution. ■

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REFERENCES

1. Hart FO: French's Index of Differential Diagnosis, ed 12. Bristol, England, J
Wright & Sons Ltd, 1985.

2. Lawson RAM, Carroll K: Delayed halitosis — A rare cause. Postgrad Med
} 1982;58(675);52-54.

3. Ballenger JJ: Diseases of the Nose, Throat, Ear, Head and Neck, ed 13. Phil-
adelphia, Lea and Febiger, 1969.

4. Paparella MM, Shumrick DA: Otolaryngology, ed 2, vol III. Philadelphia,
WB Saunders Co, 1980.

Dr Fletcher is a resident in the Dept of Otolaryngology-Head Neck
Surgery at Tulane Medical School in New Orleans.

Dr Blair is professor of Otolaryngology-Head Neck Surgery at Tulane

Medical School in New Orleans.

JOURNAL VOL 140 JUNE 9

The Advantages Of Magnetic Resonance Imaging Are Gearly Seen.

The clarity of MRI is just part of what
can be quickly seen.

Now your patients can be quickly
seen for diagnostic MR imaging as a re-
sult of East Jefferson General Hospital’s
permanent 1.5 Tesla circular polarized
magnet in our new, permanent Magnetic
Resonance Imaging Center. Because,
along with the most up-to-date MRI
technology and our staff of medical and
technical speciahsts, the center utilizes

a scheduling and report turn-around
system to make this extraordinary serv-
ice convenient for you and your patients.

MRI has proven itself. Its combi-
nation of magnetic fields, radio sound
waves and powerful computer creates
detailed images of many tissue areas we
couldn’t see as clearly before-particu-
larly in the cranial and spinal areas.

Our experience with MRI goes
beyond East Jefferson General’s new

permanent center for it. We are the
hospital that introduced this diagnostic
breakthrough to the region. And our
periodical publication, “MRI Update,”
furnishes up-to-date information on this
complicated new specialty.

So call us at 456-5154 for a per-
sonal tour of our facility, or to consult
about the possible applications of MRI
for your patients. You’ll see all its advan-
t^es. Clearly.

Mag netic Resonance Ima ging Center

East Jefferson General Hospital

Higher Standards. Outstanding Doctors.

PHOTOGRAPHY COURTESY OF SIEMENS MEDICAL SYSTEMS, INC.

Frank J. Ilardi, MD, Editor

BOOK REVIEW

PRIMARY CARE OF CANCER: Recommendations
for Screening, Diagnosis and Management
Edward A. Mortimer (ed): Case Western Reserve
School of Medicine, Cleveland, 1987, 195 pages.

by MICHAEL R. MOORE SR, MD, FACE

P RIMARY Care of Cancer, called the “Plum Book,"
is a diminutive volume when compared with its
company on the shelf of oncology reference texts. This
paperback book was written by 31 authors, mostly
physician specialists and subspecialists, from Case
Western Reserve University and the Cleveland Clinic.
The book provides concise and practical information
and is designed as a quick and ready reference for
the primary care physician encountering oncology pa-
tients.

The 29 chapters cover the 30 most common le-
sions reported to the cancer registry in the Cleveland
region, and thus reflects frequently encountered can-
cers seen in community hematology/oncology prac-
tices. Each chapter is divided into the following sec-
tions: description (containing the standard staging by
the American Joint Committee on Cancer schema, the
International Tumor, Nodal, Metastasis system, or a
disease-specific staging system), epidemiology and risk
factors, etiology, prevention, screening, signs and
symptoms, diagnostic tests, treatment and prognosis,
and post-treatment follow-up. The final chapter cov-
ers home care for the terminally iU.

The book is straightforward, pragmatic, and only
occasionally overly abridged. The Plum Book is a syn-
opsis, but does not read like a Reader's Digest con-
densed book that only skims the high points. The
sections on epidemiology, risk factors, and preven-
tion are well covered. The treatment sections are less
detailed and do not address the controversies fre-
quently encountered in oncology. In my opinion,
many treatment recommendations are overly con-
servative and fail to reflect the move to earlier and

more aggressive (frequently multimodality) therapy
being developed. In defense, however, the introduc-
tion states that “cancer therapy in the 1980s is suffi-
ciently complex that sophisticated subspecialty care
is usually indicated." The book consistently reflects
that philosophy and avoids specific and detailed treat-
ment recommendations.

I think it would have been helpful if a short bib-
liography or reading list had followed each chapter.
Also, a section describing the basics of cell growth,
oncogenesis, radiation therapy, and cancer chemo-
therapy would provide a common framework for the
discussions which followed.

This small volume, though written for the pri-
mary care physician, is packed with enough clinically
useful material to catch the interest of the hematol-
ogist/oncologist and holds its own even against the
definitive tomes on the subject. The Plum Book de-
serves its place on the shelf of any physician respon-
sible for patients with malignancy. ■

Dr Moore is a hematologist/oncologist at Willis-Knighton Medical
Center and a clinical assistant professor of medicine at
LSU School of Medicine in Shreveport.

Requests for reprints should be sent to Dr Moore, PO Box 3991,

Shreveport, LA 71133.

JOURNAL VOL 140 JUNE 11

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BOOKS RECEIVED:

The JOURNAL seeks reviews of the following books. Interested
physicians should contact Frank f. Ilardi, MD, Book Review Editor,
5000 Highway 190, Suite D-3, Covington, LA 70433.

PRACTICAL MICROSCOPIC HEMATOLOGY:

A MANUAL FOR THE CLINICAL LABORATORY
AND CLINICAL PRACTICE

Fritz Heckner, MD, H. Peter Lehmann, PhD, Yuan S. Kao,
MD; Baltimore, Urban & Schwarzenberg Inc, 1988, 97 pages.

CLINICAL ELECTROCARDIOGRAPHY:

A PRIMARY CARE APPROACH

Ken Grauer, MD, R. Whitney Curry, Jr, MD; Oradell, N],
Medical Economics Books, 1987, 544 pages.

OB/GYN EMERGENCIES: THE FIRST SIXTY MINUTES
Roy Farrell, MD (ed); Rockville, MD, Aspen Publishers Inc,

1986, 340 pages.

ENDOCERVICAL CARCINOMA:

A CERVICOSCOPIC ATLAS

Minoru Ueki, MD; St Louis, Ishiyaku Euroamerica Inc, 1987,
90 pages.

THE CLINICAL GENETICS HANDBOOK

Ruth Berini (ed); Oradell, NJ, Medical Economics Books, 1986,
385 pages.

INTERPRETING CARDIAC DYSRHYTHMIAS

Marcus Wharton, MD, Nora Goldschlager, MD; Oradell, NJ,
Medical Economics Books, 1986, 241 pages.

NEUROLOGY: PROBLEMS IN PRIMARY CARE

James L. Bernat, MD, Frederick M. Vincent, MD; Oradell,

NJ, Medical Economics Books, 1987, 656 pages.

INFORMED CONSENT: A SURVIVAL GUIDE

Donald J. Palmisano, MD, JD, Hebert J. Mang Jr, JD; New

Orleans, Invictus Publishing Co, 1987, 47 pages.

TO BE OR NOT TO BE HUMAN:

THE TFIAITS OF HUMAN NATURE

Ben Freedman, MD; New York, Vantage Press, 1987, 509

pages.

THE AGE OF MIRACLES

Guy Williams; Chicago, Academy Chicago Publishers, 1987,
221 pages.

PRIMARY CARE OF CANCER

Edward A. Mortimer Jr, MD (ed); Cleveland, Case Western
Reserve University School of Medicine, 1987, 190 pages.

HEALING INTO LIFE AND DEATH

Stephen Levine; Garden City, NY, Anchor Press/Doubleday,

1987, 290 pages.

SICKLE-CELL ANEMIA AND THALASSEMIA

Newfoundland, Canada, Canadian Sickle-Cell Society, 1987.

12 JOURNAL VOL 140 JUNE

Jackie Tucker, LSMSA President

AUXILIARY REPORT

PHYSICIANS’ HEALTH:

THE AUXILIARY’S ROLE

ELLOUISE B. SNEED

S EVERAL YEARS AGO,
the American Med-
ical Association (AMA)
and the American Med-
ical Association Auxil-
iary (AMAA) recog-
nized the need to assist
physicians and their
spouses to maintain or
regain the same health
status promoted for
their patients. With
increasing numbers of
impairment, physical
illnesses, litigation
actions, physicians leaving practice at an earlier age,
and physician suicide rates, the AMA and AMAA
implemented programs to educate physicians and their
families of available support resources. Programs were
begun to present potentially unhealthy factors af-
fecting physicians and their families. It was the AMA's
goal to relay this information with viable answers or
solutions.

The Louisiana State Medical Society (LSMS) be-
gan its first steps toward an impairment program in
1981. When the Impaired Physicians Committee of
the LSMS was granted full committee status in 1984,
the Auxiliary was given the mission of educating phy-
sician spouses about its existence and purpose. Opal
P. McBride (wife of WMam A. McBride, MD) was
instrumental in birthing this effort. Mrs McBride's
work on the Impaired Physicians Committee was
greatly influenced by the groimdwork laid by the 1975-
76 LSMSA President, Dee Cloyd (wife of William P.
Cloyd Jr, MD). Mrs Cloyd had been the first to ap-
point a Committee within the Auxiliary to promote
the health of our physicians in Louisiana.

The year 1988 finds the Auxiliary assisting in a
much broader role. The challenge is to educate. The idea
is to educate physician spouses that the best support
system is another physician spouse. Within the
framework of the Auxiliary, individual or collective
support can be given to those families experiencing
a severe physical illness, mental illness, early or reg-
ular retirement, a litigation process, or death. The
Auxiliary can assist spouses, other physicians, the ►

JOURNAL VOL 140 JUNE 13

LSMS by being a discriminate listener, by avoiding
gossip, and by being an ear to the pulse of the com-
munity's feelings.

The LSMS is encouraging each local auxiliary to
promote wellness for their members and spouses, and
to offer assistance to the local medical society in im-
plementing the LSMS Impaired Physicians Program,
Each auxiliary can begin with awareness, followed by
education, genuine concern, and encouragement for
those families experiencing distress. From these of-
fered challenges, rooted in the history of prior lead-
ership, will grow a strong health care support for the
medical family. ■

Mrs Sneed (wife of Gary A. Sneed, MD) is chairman of the
Physicians Health Committee of the LSMS Auxiliary.

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14 JOURNAL VOL 140 JUNE

Outgoing President
james W. Vildibill Jr,
MD (left) passes the
gavel and presidency
to 1 988-89 President
Daniel H. Johnson Jr,
MD at the closing
session of House of
Delegates.

he 1988 House of Delegates
convened at the 108th Annual Meeting
of the Louisiana State Medical Society on March 11-13
at the Civic Center in Lake Charles, Louisiana.

JOURNAL VOL 140 JUNE 21

EVENTS OF

Hotchkiss, MD spoke at the
Delegates Luncheon and ad-
dressed some of the major
issues facing medicine in-
cluding professional liability,
Medicare, peer review, and
the AMA's ^Congressional

LAMPAC
Fourth’'*®
District
Alternate
Director
it' 'Robert
Haley, MD
makes^a s;
presentation
the parish ^
medical
societies
participating
■a”””-,'

iM&M

alienge.

B Outgoing Auxiliary
r President Sancy
; McCool is congrat-
ulated by James W.
Vildibill Jr, MD at the
President's Dinner

LAMPAC Chairman
Howard A. Nelson,
MD outlined the
tremendous success in
electing a significant
number of LSMS sup-
ported candidates in
the recent statewide
elections.

22 JOURNAL VOL 140 JUNE

THE 108th ANNUAL MEETING

Slit

rJ;. '

.-f

■i- '.' * •

At the MecScxrfegd Pand
Discussion, David Drez,
MD (center) talks about
a hypothetical case iiv
vtdving attorneys and
physicians. Among the
oth€»' partic^^atnts wt^re
the Honorable Arthur ].
Ptanchard (left) and at-
torney' Robert Thomas
(right).

was congratulated for T7
year$ of distinguished ser-
vice as JOURNAL editor

K%/ C nna/Xkt C MFl

JOURNAL VOL 140 JUNE 23

ADDRESS OF THE

PRESIDENT

//.

Our

cohesiveness will
improve our
effectiveness in
helping to shape

social changes that can provide the
people we serve with a
better quality of life.

JAMES W. VILDIBILL JR, MD

T he past year has definitely been an
interesting one for me. 1 have
enjoyed the privilege of serving as your
president. The position has led me
down a road that personally has been
very exciting and rewarding. In this
journey over the past year, I have seen
and observed many events that are af-
fecting our lives and our profession. Let
me take just a few moments this mor-
ning to share some of my observations.

We are positively in the high-tech
age of medicine. There will no doubt
continue to be
an increase in
the number
and complexity
of real advances
in medical
technology. For
example, ad-
vantages to
physicians, and
especially our
patients, are ob-
vious in our
present ability
to eliminate
many urinary
stones with ex-
tracorporea I
shock wave
lithotripsy. This
high-technol-
ogy approach is
so much more
// satisfying than

traditional "cut-
ting for the

stone." Another
example of our
progress Is intraluminal coronary

angioplasty that often can accomplish
the same result as a coronary artery
bypass. Few, perhaps none of us,
would choose a split sternum or a flank
incision if there were an alter-

native ... and now there is.

Lots more is coming, such as im-
plantable insulin pumps that measure
out insulin in response to changing
blood sugar levels. Self-contained con-
tinuous monitoring of blood sugar
levels is an integral part of this pump.
This example is not typical of the

mega-buck, hospital-based equipment
we so frequently cite as examples of
state-of-the-art medicine.

The allure of these new and expen-
sive tools of medicine is causing a shor-
tage of physicians in small com-
munities. Increasingly, our hospitals
are the only ones who can afford many
of these advances. In many instances,
this has changed practice patterns,
often in favor of hospital-based physi-
cians. This trend could precipitate fric-
tion among physicians unless we all
think and act like physicians first, and
specialists second. We need to fight the
source of our problem, not ourselves.

GOVERNMENT'S JOB IS TO GOVERN, and it
is certainly exercising its prerogative
when it comes to medicine. Our very
success in providing quality health care
for the formerly untreatable, as well as
better health care for all, has con-
tributed significantly to the rising costs
of medical care. Government's efforts
to control these costs has resulted in a
plethora of conflicting rules and
regulations.

Professional review organizations,
set up to control Medicare costs, are
now trying to justify their existence by
controlling quality. We physicians
have serious concerns that the PRO
(Peer Review Organization)
"cookbook" approach to medicine is
having a definite influence on the
quality and level of care that is being
delivered. Despite their protests to the
contrary, I believe the PROs have
come down harder on the rural physi-
cians than they have on the remainder
of us. This makes rural practice less at-
tractive. Organized medicine must
fight for the right of all physicians.

The federal government's push to
impose DRGs (Diagnostic Related
Groups) on our radiologists,
anesthesiologists, and pathologists was
correctly seen by all of organized
medicine as an entering wedge that, if
successful, would ultimately be ap-
plied to all physicians. State medical
society, specialty society, and AMA
(American Medical Association) op-
position was successful. Organization

24 JOURNAL VOL 140 JUNE

in this instance was the key. The future
holds more government interference;
we need to be organized and ready to
combat any further government intru-
sions into the practice of medicine.

THE FUTURE QUALITY OF MEDICINE is

brighter this year in Louisiana because
of a re-invigorated State Board of
Medical Examiners working with a
strengthened Medical Practice Act. We
do not need physicians in our ranks
whose acts discredit all of medicine.
The Louisiana Board of Medical Ex-
aminers now has an enhanced ability
to effectively "disbar" these in-
dividuals. Is there a downside to this?
Surely there is. But fortunately the Loui-
siana Psychiatric Association and the
Board of Medical Examiners are
cooperatively working on rules to im-
plement our revised Medical Practice
Act. These rules will preserve physi-
cians' individual rights as well as leave
the Board the strength to deal with pro-
blems. The Louisiana State Medical
Society acted as a catalyst between
these two organizations. Such a role is
a fertile field for further activity on the
part of the LSMS. I believe the future
will bring greater understanding and
cooperation between our varied
medical organizations.

The election of Jerry Thomas, MD
as a state representative shows what a
talented and determined physician can
do with a little help from the LAMPAC
(Louisiana Medical Political Action
Committee). LAMPAC also stirred up
physician support for Governor-elect
Buddy Roemer with its "Coffee with
Representative Roemer" held at last
year's Annual Meeting. Physicians
gave an identifiable $300,000 to the
Roemer campaign, and then con-
tributed generously to his transition
team. We have every reason to believe
that medicine will have a more recep-
tive state government to work with. We
know that our legislative efforts are
conducted on behalf of our patients
and good government in general. But
persuading the often hostile Health and
Welfare Committees and then a less-
than-receptive Senate and House has

been increasingly difficult in the past
few years. We hope the situation will
improve with the anticipated change in
legislative leadership and membership.
The need for improvement is a necessi-
ty, especially as we witness the
paraprofessionals attempting to
legislatively extend their turf into the
realm of medicine. The Optometry Bill
last year would have legalized the
treatment of disease by optometrists. It
would have defined the additional
education necessary to qualify under
the law. We know the optometrists are
not going to give up their efforts. Their
defeat last year only came after ex-
haustive opposition orchestrated by
our Office of Governmental Affairs.
Sharon Knight and her staff deserve a
lot of credit. Other equally onerous
bills are coming. We need a fair shake
from our state government, and this
time I think we're going to get it.

I believe greater cooperation bet-
ween such groups as the American
Association of Retired Persons (AARP)
is in our future. This is desirable and
will benefit both medicine and a large
and growing segment of our patient
population. We have many similar
goals that will be more attainable when
coordinated with each other. J.D. Mar-
tin of Baton Rouge is responsible for
having me speak at a recent AARP state
board meeting. I came away with
good, strong vibes.

IN THE AREA OF MEDICAL LIABILITY in-
surance, I would say the future is good
for its availability to the physicians of
Louisiana. We are fortunate in having
insurers such as LAMMICO (Louisiana
Medical Mutual Insurance Company),
St Paul, the Insurance Corporation of
America, and Medical Protective. This
last company came here in June of
1 986 because of our favorable medical
tort laws dating back to Act 817 of
1975. We are fortunate to have quali-
ty companies willing to do business in
Louisiana. Availability, then, is not a
major problem for most of our
physicians.

We do have an affordability pro-
blem. Despite the fact that our liabili-

ty coverage costs in Louisiana are less
than that in two-thirds of all states, we
have some problems. These insurance
costs are great enough to raise the cost
of patient care, change practice pat-
terns, and drive needed physicians out
of practice. Physicians who have small
practices ... whether due to physical
impairment, age, and/or the need to
slow down, or who practice in im-
poverished communities where pa-
tients are unable to pay the customary
fees ... simply cannot afford to pay
liability costs. Concerned? You bet!
What is the Louisiana State Medical
Society doing about it, and what does
the future hold? In cooperation with
LAMMICO, we are playing an active
role in establishing rules for our at-
torney general's office and our com-
missioner of insurance to follow in
their administration of our Patient's
Compensation Fund (PCF). The fund
has not been run as efficiently as we
believe it should. I predict that it will
be, once these rules are established.
Some drain on our PCF is caused by
laws such as one passed several years
ago by the trial attorneys that allows ac-
tion by a plaintiff against the PCF, even
if the defendant settles for less than
$100,000. Wrong? Yes, it is; but I
predict that we can pass legislation to
correct it. Other tort laws that are not
medical in nature run up the cost of all
liability coverage, medical included.
The Collateral Source Rule prevents
the court from knowing about previous
payments and settlements to the plain-
tiff on the same issue. Our joint and
several law was modified in the last
legislature - favorably modified - but
still allows a defendant with only 507o
of the fault to be forced to pay the en-
tire judgement. I predict that these can
and will be corrected legislatively by
the Louisiana State Medical Society in
cooperation with the business
community.

Iberia Parish Medical Society has
a late resolution that I hope will be ac-
cepted by our House of Delegates. This
is a resolution to establish an En-
vironmental Committee. This may be
the key to finding out why Louisiana

JOURNAL VOL 140 JUNE 25

has the highest cancer rate second on-
ly to New Jersey in the 50 states. Our
patients are aware of this problem, we
are aware of this problem, and our
good-faith efforts to correct it will be
appreciated by the public. I predict
Louisiana will be an even better place
to live in the future.

Many of us think, perhaps with
some good reason, that public educa-
tion on health issues has only resulted
in lots of time being wasted explaining
things that formerly we did not have to
explain. Sober reflection leads me to
believe, however, that education has
got to be good if it is leavened by com-
mon sense. Public concern about ill-
understood issues manifests itself in
our mandatory pre-marital AIDS (Ac-
quired Immune Deficiency Syndrome)
testing law ... a boondoggle if there
ever was one.

Education should bean important
part of our practice of medicine.
Recognition by physicians and patients
alike of self-destructive habits and
lifestyles has already reduced our
smoking population. Another example:
a recent study showed that the simple
distribution of an elemental book on
health to a group of welfare recipients
decreased physician visits by 16%. In-
terest in health issues has never been
so high. We physicians need to be
even more involved in education and
promulgation of information that is
beneficial to our patients' health. One
test of a true professional is one who
strives to decrease the problems that
create the need for his or her services.
Dentists and their persistent teaching
of the benefits of proper dental hygiene
provide an example we could and
should make.

Many of medicine's problems are
those of society. Breakdown in family
life with an increase of "latchkey
children" as well as one-parent families
are bound to increase physical illness
as well as that increasing army of the
"worried well."

I AM NOT SO NAIVE AS TO BELIEVE that
medicine can cure all of society's ills,
nor that society can cure medicine's

problems. But as profesionals who
generally are held high in esteem by
our fellow citizens, we do bear a cer-
tain responsibility. We must be integral
members of our communities, willing
to offer our expertise and experience
to address the present and future needs
of our patients, communities, and na-
tion. The key, I believe, is to remain
strong as a profession, and to work

diligently against unwarranted and
unacceptable intrusions into the prac-
tice of medicine. We must never lose
sight of the fact that we are our pa-
tients' best health care advocates. Our
cohesiveness will improve our effec-
tiveness in helping to shape social
changes that can provide the people
we serve with a better quality of life.

26 JOURNAL VOL 140 JUNE

The LSMS honors its 50-year doctors

Pictured above:

1 . John C. Crenshaw Jr, MD, Shreveport

2. Louis A. Breffeilh, MD, Shreveport

3. Joseph M. Brocato, MD, Baton Rouge

4. Henry C. Voorhies Jr, MD, Lafayette

5. Joseph A. Sabatier Jr, MD, New Orleans

6. Collins P. Lipscomb, MD, Pontchatoula

7. David W. Vangelder, MD, Baton Rouge

8. John L. Kron Jr, MD, New Orleans

9. Myron A. Walker, MD, Baton Rouge

10. Charles L. Black, MD, Shreveport

1 1 . Oscar D. Thomas, MD, Thibodaux

12. Joe E. Holoubek, MD, Shreveport

13. Alice B. Holoubek, MD, Shreveport

14. John M. Cobb, MD, Shreveport

15. Joe D. Talbot, MD, Shreveport

16. Daniel W. Goldman, MD, New Orleans
1 7. David S. Malen, MD, Baton Rouge

18. Salvatore J. Cali, MD, Hammond

Not pictured:

A. Stirling Albritton, MD, Baton Rouge
John L. Dileo, MD, New Orleans
Homer J. Dupuy, MD, New Orleans
James H. Eddy Jr, MD, Shreveport
Frederick Eigenbrod, MD, New Orleans
Allan M. Goldman, MD, New Orleans
Bernard A. Goldman, MD, Harvey
Joseph P. Griffon, MD, Baton Rouge
N. Leon Hart, MD, New Orleans
Robert G. Heath, MD, New Orleans
Jack R. Jones, MD, Baton Rouge
William Locke, MD, New Orleans
J. Morgan Lyons, MD, New Orleans
Edward W. Nelson, MD, New Orleans
Luis R. Oms, MD, Metairie
Louis J. Supple, MD, Franklin
James E. Toups, MD, Summit, MS

JOURNAL VOL 140 JUNE 27

1988-89 ELECTED OFFICIALS

President
President-Elect
Vice President
Immediate Past President
Speaker, House of Delegates
Vice-Speaker, House of Delegates
Secretary-Treasurer

EXECUTIVE COMMITTEE

Daniel H. Johnson Jr, MD, New Orleans
Milton C. Chapman, MD, Shreveport
John C. Cooksey, MD, Monroe
James W. Vildibill Jr, MD, Lafayette
Samuel A. Leonard, MD, Metairie
R. Bruce Williams, MD, Shreveport
Howard A. Nelson Jr, MD, Marrero

Board of Councilors 6th District: Charles D. Belleau, MD (Chairman), Baton Rouge

1 St: Ronald J. French, MD, New Orleans
2nd: Frank J. George, MD, Metairie
3rd: Philip A. Robichaux Jr, MD, Raceland
4th: James R. Bergeron, MD, Shreveport
5th: David M. Walsworth, MD, West Monroe
7th: G. Michael Kent, MD, Lake Charles
8th: Leo L. Lowentritt Jr, MD, Alexandria
9th: Emile K. Ventre Jr, MD, Opelousas
10th: Stanford A. Owen, MD, Slidell

Chairman, Council on Legislation Wallace H. Dunlap, MD, Baton Rouge

Delegates

Alternates

AMA Delegates Emeriti

Young Physicians Section

AMA DELEGATION

Robert L. diBenedetto, MD, Baton Rouge
Daniel H. Johnson Jr, MD, New Orleans
A.G. Kleinschmidt Jr, MD, Marrero
Donald J. Palmisano, MD, New Orleans
Eugene F. Worthen, MD, Monroe
Terrence Beven, MD, Baton Rouge
Samuel A. Leonard, MD, Metairie
Conway S. Magee, MD, Lake Charles
W. Juan Watkins, MD, Shreveport
A. Jay Binder, MD (Resident), New Orleans
Ralph H. Riggs, MD, Shreveport
W. Charles Miller, MD, New Orleans
Gordon W. Peek, MD, Baton Rouge
Stephen L. Jolissaint, MD, Opelousas

28 JOURNAL VOL 140 JUNE

Physicians Recognition Award

Forty-nine physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
March, 1 988. This award is presented by the American Medical Association to physicians who have voluntarily
completed 150 hours of continuing medical education during a consecutive three-year time period. Of these
150 hours, at least 60 must be in AMA/PRA Category 1. These forty-nine individuals are presented below.

Abbeville

Sydney Harold Crackower, MD*

Baton Rouge

Cecil Noel Bankston Jr., MD
Willie Zachary Bienvenu, MD
Cecil W. Lovell III, MD

Brusley

Frederick Erwin Hackley, MD

Donaldsonville

Glenn David Schexnayder, MD

Franklin

Brent Wheeler Allain, MD

Gonzales

Richard Anthony Streb, MD

Gretna

Thiem Dang, MD

Harahan

Fayez H. j. Hadidi, MD*

Kinder

John James Storer, MD

Lake Charles

Ralph W. Colpitts, MD
Randall Coy Duplechain, MD
Cliff Charles Laborde Jr., MD
Richard Edward Landry, MD

Lafayette

Darrell Lane Henderson, MD
Andre Keath Perron, MD
T. Ramakrishnan, MD

Metairie

Gustavo Alberto Colon, MD
Robert Merritt de Bellevue, MD
George Gaethe, MD
Julian H. Sims, MD

Monroe

Philip Rand Warren, MD

Morgan City

Robert Paul Blereau, MD

New Orleans

Albert Barrocas, MD
Patrick John Dowling, MD*
George Wilden Hoffman, MD
Peter Robert KastI, MD
Donald Robert Lee May, MD*
Patrick Edward Mottram, MD
A. Mark Parker Jr., MD
Carlos D. Restrepo, MD*
Frank Adams Riddick Jr.,MD
Raphael Ross, MD
Beverly Ann B. Yount, MD

Oakdale

Ghanta Madhusudan Rao, MD*

Paradis

Wilson Paul Couch, MD

Pontchatoula

David Wells Bass, MD*

Shreveport

Michael O. Fleming, MD
Erie Warfield Harris, MD
William P. Kinnebrew, MD
Don Melvin Morris, MD
Milton Kenneth Scharff, MD
Daniel Richard Stevenson, MD
John Peter Valiulis, MD

Slidell

Richard Emmett Barlow, MD
Esteban Oscar Romano, MD

Ville Platte

Barney J. Fusilier, MD

West Monroe

Warren Atwood Daniel Jr., MD

* These individuals are not members of the Louisiana State Medical Society.

JOURNAL VOL 140 JUNE 33

HEART TRANSPLANTATION

THE LOUISIANA EXPERIENCE

JOHN L OCHSNER, MD; CLEMENT C. EISWIRTH JR, MD

34 JOURNAL VOL 140 JUNE

The renewed Louisiana experience in cardiac
transplantation now spans more than two years.
During this period, 27 patients have received
transplanted hearts. Improved measures in
immunology, organ preservation, and the detection
and treatment of rejection have favorably affected
the outcome. The results in this experience are
exceptionally good. There is a 93% one-year
survival and in each patient the cardiac status has
reverted to New York Heart Association Class I.
The expectation of excellent long-term survival
warrants continued efforts to treat selected patients

in end-stage heart disease.

O NE OF THE most spectacular medical achievements
was in 1967, when Dr. Christian Barnard re-
ported the first successful human cardiac transplan-
tation.^ In the next few years, we and many centers
performed either isolated or a limited number of car-
diac transplants. This early experience was disap-
pointing since the majority of patients died within the
first post-transplant year. Hence, the procedure was
considered experimental and, except for the contin-
ued efforts by the Stanford University and the Medical
College of Virginia groups, the medical profession
self-proclaimed a moratorium on cardiac transplan-
tation. However, since 1982, there has been a re-
newed interest in the procedure due to significant
advances in immunosuppression, patient selection,
myocardial preservation, diagnosis of rejection, and
a better understanding of patient management. Uti-
lizing these advances, more and more institutions have
re-entered or initiated programs. Today there are 84
cardiac transplantation centers in the United States
and more than 30 in other countries. There were 800
cardiac transplantations performed in 1985 with cur-
rent statistics indicating an 80% one-year survival and
70% two-year survival.^ The Ochsner Clinic renewed
its cardiac transplantation program on September 4,
1985, and the first transplant was performed on Oc-
tober 30, 1985. The stimulus for development of the
program was determined by a definite need for a car-
diac transplantation center in our geographic region.
The ability to institute this program was a natural
extension of an established kidney and bone marrow
transplantation program and an ongoing active multi-
faceted open-heart program.

^ 4 ^ JAble 1

CRITERIA FOR ELIGIBILITY AS A CARDtS;
TRANSPLANT RECIPIENT

1. Severe, Class ill or IV cardiac dysfunction unremedial to
surgical treatment other than cardiac replacement

2. Limited life expectancy, with a one-year mortality estimated
to be > 50%

3. Physiologic age < 60 years; absolute upper limit for
chronologic age is 65

4. No systemic illness other than abnormalities related to
heart failure

5. Emotional stability

6. Strong family support system

7. Absence of the following exclusion criteria:

a. Severe pulmonary hypertension (PVR > 8 wood units
or PVR > 6 wood units with inability of nitroprusside
infusion to reduce PVR to below 3 or inability to
reduce PA systolic below 50 mmHg

b. Severe, irreversible hepatic, renal or pulmonary
disease

c. Active systemic or pulmonary infection

d. Recent pulmonary infarction

e. Insulin-dependent diabetes

f. History of uncontrollable hypertension, defined as
blood pressures consistently greater than 160/100 mm/
Hg on medical therapy

g. Systemic vascular or cerebral vascular disease

h. Active peptic ulcer disease

i. History of substance abuse (including alcohol) or
behavior problem

PVR: pulmonary vascular resistance
PA: pulmonary artery

CLINICAL DATA

We have received numerous phone calls on behalf of
potential recipients. Screening at this level determines
the suitability of the patient, resulting in a higher
acceptance percentage of patients actually referred.
The criteria for acceptance are shown in Table 1. Fifty-
seven patients have been referred for cardiac trans-
plantation (Table 2), 16 of which were rejected. Rea-
sons for exclusion are listed in Table 3. One patient
who would have been an acceptable candidate based
upon initial screening declined further consideration
and was lost to followup. One patient had a history
of being a recovered alcoholic who had joined Alco-
holics Anonymous and gained the support of his fam-
ily. He was rejected because of a brachial cleft fistula
which prevented sterile entry into the right jugular
vein. Due to technical difficulty, alternative biopsy

JOURNAL VOL 140 JUNE 35

TABLE 2

CARDIAC TRANSPLANTATION —

PATIENT PATTERN

Referred for transplantation

Rejected (medical and social)

Died awaiting transplant

Received transplantation

Awaiting transplantation

routes are not amenable to the repeated entries nec-
essary to obtain multiple biopsy specimens. Since this
is so important for adequate management of the car-
diac transplant patient, he was rejected.

Two additional patients died while awaiting
transplantation, one of cardiogenic shock after being
transferred for emergent cardiac transplantation when
no donor could be located, and the other of congestive
heart failure following a pulmonary embolus which
had made him an unsuitable candidate.

Twenty-seven patients have undergone cardiac
transplantation. There were 22 males and 5 females,
and their ages ranged from 12 to 60 (mean 45.2, me-
dian 48). The primary cardiac diseases in these pa-
tients were as follows: ischemic cardiomyopathy in
14, idiopathic cardiomyopathy in 10, congenital heart
disease in 2 and rheumatic valvular cardiomyopathy
in 1.

The referrals have come from a wide base in-
cluding Texas, Mississippi, and Alabama. Of the 27
patients receiving transplants, 19 (70.4%) were from
Louisiana, 6 (22.2%) from Mississippi, and 2 (7.4%)
from Alabama. All patients were in New York Heart
Association Classification III or IV.

Donor hearts were obtained from many different
locations in five states. The ischemic time ranged from
59 minutes to three hours and 14 minutes (average
one hour and 54 minutes).

A careful surgical and medical evaluation was
done on all patients. Two patients were on intra-aortic
balloon counterpulsation in order to maintain suffi-
cient hemodynamics to transport them to the oper-
ating room. Four hospitalized patients required vaso-
active drug infusions to stay alive. Two patients had
cardiac arrest during the induction of anesthesia and
were immediately placed on extracorporeal circula-
tion.

TABLE 3

REASONS FOR EXCLUSION FROM
CARDIAC TRANSPLANTATION

Pulmonary hypertension 2

Diabetes 2

Severe peripheral vascular disease 2

Poor medical compliance 2

Poor social support 2

Substance abuse 2

Active infection 1*

Cerebrovascular accident (recent) 1 *

Severe systemic hypertension 1

Inability to biopsy 1

Patient declined 1

* Same patient

In addition to the transplantation medical and
surgical teams, these patients were evaluated by clin-
ical psychiatry, nursing, social services, and pastoral
service. Of the 27 patients receiving transplants, 25
were listed on national computer systems to await a
suitable donor.

Immunosuppressive therapy varied according to
the patient's individual problems and the availability
of drugs. In general, two different protocols have been
followed. In both protocols, triple drug therapy con-
sisting of cyclosporin, azathioprine (Imuran®), and
steroids was used. In one group, the use of antilym-
phocyte globulin in the preoperative and early post-
operative period was added to this triple therapy. In
general, cyclosporin levels are maintained above 75
ng/mL, as measured by high pressure liquid chro-
matoptometry technique. Imuran® is progressively
lowered to a daily maintenance dose of 1.0 mg/kg to
2.0 mg/kg, and prednisone is tapered to a mainte-
nance dose of 0.1 mg/kg to 0.15 mg/kg.

All patients have undergone repeated endomy-
ocardial biopsies. These are scheduled every week for
the first six weeks, then every two weeks for the next
six weeks, then every month for three months, then
every two months for six months, and every three
months thereafter.

RESULTS

Twenty-seven patients have received transplants with

36 JOURNAL VOL 140 JUNE

a followup of one week to 25.5 months (mean 9.4
months). There have been no operative deaths and
only two late deaths (Fig). The first death was in a
12-year-old boy who, in his sixth month following
transplantation, developed gastroenteritis and during
a three-day period was unable to maintain his oral
intake of immunosuppressive drugs. He had an acute
rejection. He arrived at the hospital in cardiogenic
shock and required extracorporeal membrane oxy-
genation to maintain life. His rejection was reversed
with steroid and antilymphocyte globulin. He devel-
oped fatal disseminated aspergillosis with extensive
central nervous system involvement. The other death
occurred in a man who developed Pneumocystis carinii
pneumonia two months following transplantation. He
subsequently developed disseminated cytomegalo-
virus infection, bacterial sepsis, and renal failure and
died 30 days after presentation with infection. The
remaining 25 patients are alive. Thus, the actuarial
one-year survival in this series is 93% .

Fourteen patients have been followed for six
months to 25.5 months (mean 16.2 months, median
16.5 months). Of these patients, only the 12-year-old
died. While it is too early to project a meaningful two-
year survival, these data suggest that mortality be-
yond six months may not increase substantially though
a longer followup wiU be needed. This is consistent
with the reports of the Transplant Registry.

Complications have been relatively few. Two pa-
tients developed superficial wound infections (one
chest and one groin) requiring open drainage with
subsequent healing by secondary intention. One week
postoperatively, one patient developed an episode of
cerebral ischemia which spontaneously resolved. An-
other patient remains in the hospital without the need
of support, but with significant cerebral impairment.
During the postoperative period, five patients devel-
oped oral candidiasis and/or herpes simplex, all of
which resolved within the first month. Three patients
developed herpes zoster, two with a single derma-
tome and one with multiple dermatome involvement.
Atrial fibrillation required treatment in two patients.
There were two hemodynamically significant epi-
sodes of rejection and one pulmonary embolus. There
were three serious infections: one patient with dis-
seminated aspergillosis and two patients with pneu-
monia.

REJECTION

Cardiac rejection is generally termed mild if only peri-

Fig. Length of followup of 27 cardiac transplant
recipients.

Number of months

vascular infiltrates are present, moderate if there is
interstitial extension, and severe if the infiltrate is ex-
tensive and mycotic necrosis is present within the
areas of the infiltrates. With the use of cyclosporin,
many patients develop cardiac fibrosis (which is not
clinically relevant) and lymphocytic perivascular in-
filtrates without clinical sequelae. For this reason, most
programs only treat patients who develop interstitial
extension unless clinical features suggest the need to
treat a lesser degree of infiltration.

Cardiac rejection is most frequent within the first
six months following transplantation. In our series,

14 patients followed for at least six months developed
18 rejections for an average of 1.3 rejections/patient.
Only two patients demonstrated rejection after the
first six months. One of these is a poorly compliant ►

JOURNAL VOL 140 JUNE 37

BECAUSE

ONLY

VALIUM

VALIi

Vw/

IS ALWAYS W jUM

REMEMBER TO WRITE “DO NOT SUBSTITUTE.”
IT PROTECTS YOUR DECISION.

The cut out "V" design is a registered trademark of Roche Products Inc.

patient who has had a total of three rejections, with
two of these occurring seven months and 17 months
following transplantation. The other patient had no
rejections within the first year following transplan-
tation but subsequently developed three episodes.
Both are currently without rejection at 18.5 months
and 16.5 months of followup, respectively.

Overall, the 27 patients have developed 32 epi-
sodes of rejection. This yields 1.2 episodes of rejec-
tion/patient with a mean followup of 9.4 months, me-
dian 6.0 months.

All patients who received transplants are now
New York Heart Association Class I. Many have re-
turned to their previous occupations or are receiving
retraining in another occupation. Three patients have
moderate degrees of renal insufficiency with serum
creatinines of 1.7 mg% to 2.2 mg%. All but three
patients have developed hypertension secondary to
cyclosporin and are receiving antihypertensive ther-
apy.

DISCUSSION

Over 3,000 heart transplants have been performed
worldwide. More than one-half of these were per-
formed in the past two years. The effects of trans-
plantation on quality of life can be dramatic. In terms
of cardiac status, improvement from New York Heart
Association Class III-IV clinical condition to Class I
has occurred in all our patients. Transplanted hearts
have demonstrated excellent function. Despite de-
nervation, the heart displays normal contractility and
contractile reserve.

The limitations placed on isolation of recipients
has become more lenient as experience increases and
results improve. The age of recipients has progres-
sively increased and the late survival for patients 50
to 65 years of age is similar to that of patients under
50 years of age.

Today, the national one-year survival is 80% and
the two-year survival is 65%. The survival of our pa-
tients has been excellent. A total of 91% have survived
one year. Our two-year survival rate will require a
longer followup. Thus far, all patients surviving six
months following cardiac transplantation remain alive
at followup of six months to 25.5 months (mean 16.2
months, median 16.5 months). A close interrelation-
ship of all concerned in the various stages of the care
of these extraordinarily complicated patients is essen-

tial to a successful outcome. The selection and prep-
aration of recipients, the procurement of the donor
organs, the operative implantation of the organs, and
the immediate and late postoperative therapy should
be synchronized in order to achieve maximum ben-
efit. A full-time cardiac transplantation service best
meets these needs, and frequent conferences which
include all members of the team serve to communicate
the essential requirements of various members and
their patients.

In the early days of transplantation when im-
munosuppression relied on multiple courses of high-
dose steroid therapy, patients were vulnerable to an
extremely high rate of infection. The advent of cy-
closporin and its immunosuppressive efficacy has been
a- major breakthrough in the prevention of life-threat-
ening infections. Moreover, the knowledge gained in
the use of many different immunologic agents has led
to a better understanding of patient management. The
use of multiple agents, combined in such a manner
as to maintain patients on a dosage of each drug low
enough to not excite complications, has allowed long-
term survival without increased hazards from the
drugs. The continued development of new drugs
combined with a better knowledge of immunology
should continue to provide better means to control
rejections.

Monitoring the immune system by way of pe-
ripheral blood is a useful support mechanism for car-
diac transplantation. Immune monitoring with mono-
clonal antibodies and flow cytometry may be useful
as an adjunct study in the early diagnosis of infection,
allograft rejection, and malignant clonal proliferation
of B cells. We have observed that up to two weeks
before an allograft rejection occurs, peripheral blood
lymphocyte subsets express activation antigens such
as the transferrin receptor. Expression of activation
antigens on the peripheral blood lymphocytes in an
immunosuppressed cardiac transplant patient greatly
increases the risk for an allograft rejection episode.

An increased Helper T/Suppressor T ratio (normal 1.8)
also increases the risk of a rejection episode. The
T Helper population has two important functional
subsets: 1) the helper inducer subset, which is im-
portant in regulating activation of the immune sys-
tem; and 2) the suppressor inducer subset, which is
important in regulating suppressor effector activity of
the immune system. We have observed a relative def-
icit of the suppressor inducer subset during rejection ►

JOURNAL VOL 140 JUNE 39

ACKNOWLEDGMENTS

episodes but not during infection episodes. During
viral infection, we have observed a severely decreased
Helper T/Suppressor T ratio together with a signifi-
cant HLA-DR activation of T cells. One may expect
to see a significantly increased Helper T/Suppressor
T ratio during bacterial infections, especially Staphy-
lococcus infections. For the future, we can anticipate
that monoclonal antibodies will play an ever-increas-
ing role in the treatment of rejection episodes. The
same monoclonal antibody that is now used to detect
activated lymphocyte subsets as a means for early
diagnosis of rejection episodes can potentially be em-
ployed in the treatment of cardiac transplant recipi-
ents.

In the formulative years of cardiac transplanta-
tion, the methods and means to determine rejection
were crude and inaccurate. The development and use
of endomyocardial biopsy has proven precise in the
diagnosis of rejections. Grades of rejection and, con-
sequently, the need and degree of therapy can be
ascertained. This information has been of immeas-
urable assistance in determining the need for treat-
ment and control of rejection.

Newer methods of myocardial preservation have
helped to increase the supply of organs by allowing
more time from procurement to transplantation. Thus
logistics have improved since organs can travel longer
distances, and more time is allotted to the technical
aspects of the operation.

In conclusion, the first two years of renewed car-
diac transplantation at the Ochsner Clinic have dem-
onstrated significant activity. Patient survival is con-
siderably better than the national average, and the
rate of infection and rejection is likewise well con-
trolled. The recipients have been able to return to
active and productive lives. This successful experi-
ence warrants continuation of this endeavor. ■

Many individuals have participated in the care of the
cardiac transplant patients and we wish to recognize
some: Dr Clark Springgate, Dr John L. Hussey, Dr
Walter Culpepper, Dr Luther Williams, Dr Nelson
Ancalmo, Dr Noel Mills, Dr Michael Horowitz, Dr
John Busby, Dr James Gilmore, Dr Tommy Fudge, Dr
Shannon Cooper, Dr Donald Harmon, Dr Robert Mar-
ino, Dr Peter Stedman, Mr Frank J. Heckenkemper,
Mr William T. Stevenson, Miss Ellen Badeaux, RN,
and Miss Debi Dumas, RN.

REFERENCES

1. Barnard CN: Human cardiac transplant: An interim report of a successful
operation performed at Grote Schuur Hospital, Cape Town. S Afr Med J
1976;41:1271-1274.

2. Kaye MP: The International Heart Transplantation Registry, 1984 report.
Heart Transplantation 1985;4:290-292.

Dr Ochsner is from the Dept of Surgery at Ochsner Clinic and Alton
Ochsner Medical Foundation in New Orleans.

Dr Eiswirth is from the Dept of Internal Medicine, Section on
Cardiology at Ochsner Clinic and Alton Ochsner Medical Foundation in

New Orleans.

Reprint requests should be sent to Dr John Ochsner, Ochsner Clinic,
1514 Jefferson Hwy, New Orleans, LA 70121.

40 JOURNAL VOL 140 JUNE

MICROSURGERY IN BREAST
RECONSTRUCTION USING THE
SUPERIOR GLUTEUS FOR
FREE TISSUE TRANSFER:

A CASE REPORT

MARY LYN T. LU, MD; WILLIAM M. SWARTZ, MD

The gluteus free flap breast reconstruction is
presented as an alternative to other methods,
including tissue expands and the transverse
abdominal flap. The principal reasons to consider
this method are the availability of adipose tissue
in the gluteal region, even in thin patients, and the
well-tolerated donor site. The authors' preference
for early reconstruction is based on data which
indicate that most local recurrences do not occur
until after the accepted two-year interval.

B reast cancer is the most frequent malignancy in
women, with a progressive rise in incidence after
the third decade of life. In the United States alone,
approximately 40,000 radical mastectomies are per-
formed each year.^

While most of the women who undergo mastec-
tomy are able to adjust, studies have shown that there
is a definite psychological effect of mastectomy.^ The
four most common categories are depression lasting
for months to years, lowered self-esteem, diminished
sense of femininity, and panic imposed by the po-
tentially lethal cancer. The greatest benefit of breast
reconstruction is improving the patient's sense of well
being. Restoration of the breast form increases the
patient's feelings of femininity, decreases self-con-
sciousness and embarrassment, and improves overall
appearance, with relief from clothing and prosthetic
problems.^' 2

The timing of breast reconstruction varies mostly
due to physician bias. Immediate reconstruction at
the time of mastectomy or within the first week post-
operatively is gaining acceptance in Stage I disease.^
Some physicians prefer to wait two years with the
belief that 80% of local recurrence develops within
two years. There are reports in the literature^' ^ that a ►

JOURNAL VOL 140 JUNE 43

two-year delay in breast reconstruction is not justified
and is without oncologic advantage because in Stage
I disease, the mean disease-free interval is 6.2 years
and it takes 10 years for 80% of recurrences to ap-
pear.^' ^ Our preference is to perform immediate re-
construction when feasible. Delayed reconstruction as
soon as the patient's post-mastectomy scars are soft-
ened (usually within six months of surgery) is a rea-
sonable alternative to waiting two years. For patients
undergoing chemotherapy, reconstruction is per-
formed following recovery of the white blood count
in an interval between treatments.

CHOICE OF METHOD

Recent advances in breast reconstruction have pro-
vided a variety of methods that can be adapted to
each patient's needs.

For immediate reconstruction, the most fre-
quently performed procedure is the tissue expander,
later exchanged for a permanent prosthesis of slightly
smaller size at a second procedure. Newer permanent
expanders are available, thereby obviating a second
procedure. While this method is probably the easiest
on the patient, it has certain drawbacks. Frequently,
it is not possible to match the opposite breast in size
and contour. In many of these reconstructions, cap-
sular contractures around the implant necessitate im-
plant exchange or removal. Finally, adequate soft tis-
sue coverage may not be present in patients requiring
wide skin excision.

To obviate the problems associated with pros-
thetic reconstruction and to match the contralateral
ptotic breasts, the Transverse Rectus Abdominal Mus-
culocutaneous Flap (TRAM), based on the superior
epigastric pedicle, was developed by Hartrampf.^ The
TRAM flap provides autogenous tissue with an ad-
equate volume for the largest breast mound and gives
the added benefit of flattening the abdomen. With
this procedure, there is a possibility of weakening the
abdominal wall due to sacrifice of the rectus muscle.
It is not recommended for obese patients or heavy
smokers and may be_ contraindicated in the presence
of multiple abdominal scars that impair blood supply
to the flap. It is not ideal when there is an inadequate
abdominal panniculus or if pregnancy is desired at a
later time.

To overcome the limitations of the previous pro-
cedures, the superior gluteus myocutaneous flap as

Fig 1. Preoperative view. Note size and ptosis of

contralateral breast.

a free tissue transfer was first reported by Fujino^ and
later refined by Shaw.® The superior gluteus myocu-
taneous flap provides autogenous tissue, which, like
the TRAM flap, is soft and simulates normal breast
tissue. Even in thin patients, there is always adequate
tissue for breast reconstruction and the scar, hidden
from the patient's normal view, is cosmetically ac-
ceptable. Sacrifice of a portion of the gluteus muscle
does not impair function of the remaining muscle,
and the contour change is minimal. Although this is
a relatively long procedure with the need of special
facilities and microsurgical techniques, it provides a
reliable and aesthetically acceptable reconstruction in
problem patients.

CASE REPORT

A 30-year-old female with a Stage I infiltrating in-
traductal carcinoma had a right modified radical mas-
tectomy. She did not want to have a prosthetic re-
construction. Her abdomen was flat, without a good
panniculus, and she wished to become pregnant at a
later time. Six months post-mastectomy, she was re-
constructed with a superior gluteus myocutaneous
free tissue transfer. The superior gluteal artery and
vein were anastomosed to the internal mammary ar-
tery and vein with a vein interposition graft. Three

44 JOURNAL VOL 140 JUNE

Fig 2. Postoperative view. Nipple areolar complex
reconstructed with quadripod flap and free
skin graft. Contralateral breast was elevated
with a mastopexy.

months after the mound reconstruction, she under-
went a nipple areola complex reconstruction using a
quadripod flap for the nipple and a full-thickness skin
graft for the areola. The left breast required a mas-
topexy for final symmetry (Figs 1-3).

SUMMARY

Immediate reconstruction for early breast cancer has
important psychological benefits that should be con-
sidered in the patient's overall treatment plan. Per-
forming a reconstruction before the standard two-year
delay has not been shown to increase the incidence
of local recurrence or hinder its detection and treat-
ment.^' ^

There are several options in breast reconstruction
with individual benefits and limitations. An autoge-
nous breast mound with adequate volume that
matches a ptotic contralateral breast in shape, vol-
ume, and firmness is the reconstructive goal. The su-
perior gluteus mycocutaneous free tissue transfer is
presented as a reasonable alternative to the transverse
abdominal island flap.

The principal advantage lies in the quality of the
donor site which is most acceptable from an aesthetic

Fig 3. Donor site following gluteus myocutaneous
flap breast reconstruction.

and functional point of view. For patients in whom
other methods of reconstruction are neither possible
nor acceptable, the gluteus free flap breast reconstruc-
tion becomes the procedure of choice. ■

REFERENCES

1. Coin JM, Coin MK: Changing the Body — Psychological Effects of Plastic
Surgery. Baltimore, Williams and WUkms, 1981, pp 163-189.

2. Snyderman RK: Reconstruction of the Breast After Surgery for Malignancy,
Goldwyn RM (ed). Boston, Little Brown and Co, 1976; pp 465-479.

3. Noone RB, Murphy JB, Spear SL, et al; A six-year experience with im-
mediate reconstruction after mastectomy for cancer. Plast Reconstr Surg
1985;76:258-269.

4. Dowden RV, Blanchard JM, Greenstreet RL: Breast reconstruction — Se-
lection, timing and local recurrence. Ann Plast Surg 1983;10:265-269.

5. GBLUand MD, Larson DL, Copeland EM: Appropriate timing for breast
reconstruction. Plast Reconstr Surg 1983;72:335-337.

6. Hartrampf CR, Scheflan M, Black PW: Breast reconstruction with a trans-
verse abdominal island flap. Plast Reconstr Surg 1982;69:216-224.

7. Fugino T, Harshima T, Aoyad F: Reconstruction for aplasia of the breast
and pectoral region by microvascular transfer of a free flap from the
buttock. Plast Reconstr Surg 1975;56:178-181.

8. Shaw WW: Breast reconstruction by superior gluteal microvascular free
flaps without silicone implants. Plast Reconstr Surg 1983;72:490-499.

Drs Lu and Swartz are from the Dept of Surgery, Division of Plastic
Surgery, at Tulane Medical School in New Orleans.

Reprints will not be available.

JOURNAL VOL 140 JUNE 45

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SURGICAL MANAGEMENT
OF IMPOTENCE:

NEW MODALITIES

NEIL BAUM, MD

Impotence is a common problem affecting millions
of Amerian men. Of these, 50% are impotent on
the basis of physical or organic causes. This article
reviews the most recent advances in the surgical
management of impotence.

T wenty years ago, most patients with impotence
were considered to have psychogenic or emotional
causes for their sexual dysfunction. Following the pi-
oneering work of Masters and Johnson and with the
assistance of new diagnostic techniques, nearly 50%
of all impotent patients have been found to have an
organic or physical cause of their erectile dysfunction.

In the past, most cases of organic impotence were
treated with testosterone injections and penile
prostheses. This article reviews new modalities of sur-
gical management of impotence.

VASCULOGENIC IMPOTENCE

Arterial Insufficiency

In 1923, Leriche recognized the relationship between
arterial insufficiency and erectile dysfunction.^ The
clinical syndrome he described consisted of claudi-
cation in the lower extremities, buttock pain, and im-
potence. The pathology consisted of occlusion of the
distal aorta or the common iliac arteries. Since that
initial report, very little had been done in treating
vasculogenic impotence until the 70s. Now, with a
better imderstanding of vascular pathophysiology and ►

JOURNAL VOL 140 JUNE 47

new diagnostic tests to identify vasculogenic impo-
tence, effective treatment for this common cause of
impotence is on the horizon.

The arterial blood supply to the penis originates
from the hypogastric artery and the internal pudendal
artery. The internal pudendal supplies the common
penile and finally the dorsal penile and the cavernosal
arteries. With appropriate pelvic nerve stimulation,
arteriolar resistance decreases and the blood supply
to the corpora cavernosa subsequently increases with
resulting tumescence and rigidity. With occlusion at
either the proximal or distal end of the blood supply,
penis erectile dysfunction can occur. Patients with
arterial occlusive disease have a history of progressive
loss of tumescence and rigidity, and nocturnal penile
tumescence testing (NDT) shows decreased or absent
nocturnal erections.

There is one disorder described as “pelvic steal
syndrome" in which the patient can obtain an erection
but fail to maintain it after vaginal penetration and
pelvic thrusting.^ Patients with pelvic steal syndrome
have normal NPT tests and can maintain the erection
when the male is in the inferior or supine position.
The arterial occlusion in pelvic steal syndrome occurs
at the level of the external iliac or the hypogastric
artery. These patients can obtain an erection, but with
physical exertion, the blood supply is subtracted or
"stolen" from the erectile bodies and diverted to the
muscles of the pelvis and lower extremities resulting
in detumescence.

The diagnostic tests for vasculogenic impotence
begin with noninvasive tests such as the Doppler pe-
nile blood pressure determination. The penile blood
pressure is indexed against the brachial artery blood
pressure. A normal penile-brachial index is 1.0 and
an index <0.6 is highly suggestive of arterial insuf-
ficiency. If the history and the Doppler study suggest
arterial insufficiency and the patient is a candidate for
a revascularization operation, then the location of the
occlusion is identified by selective internal pudendal
angiography.

Vascular insufficiency can be divided into two
treatment categories: proximal occlusive disorders and
distal occlusive disorders.

Proximal disorders involve the distal aorta, com-
mon iliac arteries, or the hypogastric arteries. Man-
agement of proximal occlusive disorders includes
standard graft bypass procedures, endarterectomies,

48 JOURNAL VOL 140 JUNE

Fig 1. Dynamic corpora cavernosogram demon-
strating venous leak (arrow).

and, currently, the use of transluminal balloon an-
gioplasties.^

Distal occlusive disorders have been successfully
treated with revascularization procedures using op-
tical magnification. There are a variety of techniques
to accomplish the revascularization of the distal penile
arterial blood supply. Most of these techniques are
based on either 1) anastomosis of the inferior epigas-
tric artery directly to the corpora cavernosa or to the
deep dorsal vein of the penis and then creation of an
anastomosis between the arterialized vein and the
corpora cavernosa, or 2) arterialization of the patent
distal penile arteries. The successful results of these
revascularization procedures vary from 30% to 80%.^
The most successful results occur in the younger pa-
tient who has vasculogenic impotence on the basis of
pelvic or perineal trauma.

Venous Incompetence

Ligation of the dorsal vein of the penis, reported at
the turn of the century, was one of the first surgical
approaches in the treatment of impotence.^ This pro-
cedure did not meet with significant success and was
abandoned. Recently, the importance of the venous

system in the physiology of erection has become ap-
parent and new diagnostic techniques have been de-
veloped to identify abnormal venous drainage leading
to correction of abnormal venous drainage from the
corpora cavernosa.

Studies on the physiology of an erection have
demonstrated that the venous outflow from the cor-
poral bodies decreases during erection. When there
is a failure to decrease this venous outflow from the
erectile bodies, a "venous leak" situation occurs and
there will be failure to trap the blood supply in the
penis. ^ Patients with venous leak have a history of
partial erections, lacking the rigidity for adequate vag-
inal penetration. Often the patients describe "stuff-
ing" the partially erect penis into the vagina. Venous
leak impotence is one of the few physical causes of
primary erectile dysfunction.

The diagnosis of venous leak impotence is made
by dynamic corpora cavemosography.^ This tech-
nique consists of infusion of contrast material into the
corpora cavernosa and measurement of the pressure
within the corpora cavernosa together with simulta-
neous fluoroscopic monitoring, when tumescence or
erection occurs. The criteria for venous leak by this
diagnostic procedure include: 1) excessive inflow rates
necessary to produce an erection, 2) early visualiza-
tion and dilatation of the veins draining the corpora
cavernosa (Fig 1), and 3) early washout of the contrast
material from the corpora cavernosa.

The treatment of venous leakage consists of li-
gation of the abnormally draining veins and their trib-
utaries. Nearly 50% to 75% of the patients with doc-
umented venous leak will have improvement in their
erections following surgical ligation of the abnormal
veins.®

PEYRONIE'S DISEASE

Peyronie's disease or "bent penis" deformity is a com-
mon cause of erectile dysfunction. The etiology of the
fibrosis or scar formation replacing the erectile tissue
within the corpora cavernosa is unknown. There have
been numerous conservative approaches to this prob-
lem none of which has been uniformly successful.^ It
is difficult to assess conservative management be-
cause many cases of Peyronie's disease undergo spon-
taneous remission. The indications for surgical cor-
rection of Peyronie's disease include: 1) persistent
deformity for longer than one year, 2) significant de-

formity that makes vaginal penetration difficult or
painful to either the patient or his partner, and 3)
painful erections. The techniques available for cor-
rection of Peyronie's disease include plaque excision
and replacement with either a dermal graft or a syn-
thetic material such as Dacron. These procedures are
used if there is minimal replacement of the erectile
tissue with scar formation and the patient is potent.

If there is significant replacement of the erectile tissue
and the patient is impotent, then one of the penile
prostheses is inserted after removal of the fibrous
plaque.

PENILE PROSTHESES

In the late 60s the first serriirigid rod (SRR) penile
prosthesis was made available for the treatment of
impotence. This prosthesis was effective in creating
an erection adequate for vaginal penetration. How-
ever, the SRR is associated with a permanent erection
that causes problems with concealment and psycho-
logical acceptance. In the early 70s, Dr F. Brantley
Scott developed the inflatable multicomponent penile
prosthesis. This device consisted of two inflatable
cylinders that were inserted into the corporal bodies,
a pump that is inserted into the scrotum, and a res-
ervoir placed behind the pubic symphysis. This pro-
duces a natural-appearing erection that increases in
both girth and length when the device is inflated and
a flaccid penis when the device is deflated. As a result,
the inflatable perule prosthesis does not cause prob-
lems with concealment or acceptance.

As in most areas of medicine, new technology
has resulted in improvements in the devices and in
simplification of surgical procedures. Currently, there
are two brands of self-contained penile prostheses:
Flexi-Flate® (Surgitek, Racine, Wis) and Hydro Flex®
(American Medical Systems, Minnetonka, Minn). One,
the Hexi-Hate, consists of two hydraulic cylinders each
containing a reservoir located directly behind the in-
flate/deflate mechanism (Fig 2). This prosthesis offers
the advantages of rigidity and flaccidity but with less
difficulty in implantation than the multi-component
inflatable penile prosthesis.

A new mechanical device has been developed
that does not use the hydraulic principle of moving
fluid by a pump mechanism between a reservoir and
cylinders within the corpora cavernosa. This Omni-
phase prosthesis (Dacomed Corp, Minneapolis, Minn) ^

JOURNAL VOL 140 JUNE 49

Fig 2. Self-contained inflatable penile prosthesis (photo courtesy of Medical Engineering Corp, Racine,
Wis).

>■

/■

Fig 3. Omniphase prosthesis (photo courtesy of Dacomed Corp, Minneapolis, Minn)

consists of a mechanical cable which is attached to an
activating mechanism within the prosthesis (Fig 3).
The prosthesis can be activated by bending the penis
downward toward the scrotum. When the penis is
released, the device becomes rigid and adequate for
intercourse. The device is deactivated by repeating
the process and the penis becomes flaccid.

Soon to be marketed is the Girth, Placidity, Sim-
plicity (GFS) Prosthesis® (Mentor, Goleta, Calif) which
will provide the most natural erection and which will
also be easy to surgically implant. This is a two com-
ponent hydraulic inflatable prosthesis consisting of
cylinders inserted into the corporal bodies of the penis
and a combination pump-reservoir component that is
placed dependency within the scrotum. This device
provides the rigidity and flaccidity of the Scott pros-
thesis together with the simplicity of insertion as the
semirigid rod prosthesis,

SUMMARY

The management of organic impotence has developed
dramatically in the last few years. It is possible to
accurately diagnose most causes of impotence and to
effectively treat almost all patients with this common
problem. ■

REFERENCES

1. Leriche R: Des obliterations arterielles hautes comme cause d'une in-
suffisance circulatoire des membres inferiers. Bull Soc Chirurgie
1923;49(33):1404-1406.

2. Goldstein 1, Siroky MB, Nath RL, et al: Vas-
culogenic impotence; Role of the pelvic steal
test. / Urol 1982;128(2):300-306.

3. Goldwasser B, Carson CC, Braun SD, et al. Im-
potence due to the pelvic steal syndrome: Treat-
ment by Uiac transluminal angioplasty. / Urol
1985;133(5):860-861.

4. Goldstein 1: Arterial revascularization proce-
dures. Semin Urol 1986;4(4):252-258.

5. Wooten JS: Ligation of the dorsal vein of the
penis as a cure for atonic impotence. Tex Med
1903;18(8):325-328.

6. Wagner G: Erection: Physiology and endocri-
nology, in Impotence: Physiological, Psychological,
Surgical Diagnosis and Treatment, Wagner G,
Green R (eds). New York, Plenum, 1981, 25-36.

7. Puyau FA, Lewis RW: Corpus cavemosogra-
phy: Pressure, flow and radiography. Invest Ra-
diol 1983;18(6):517-522.

8. Lewis RW, Puyau FA: Procedures for decreas-
ing venous drainage. Semin Urol 1986;4(4):263-
272.

9. Mira JG: Is it worthwhile to treat Peyronie dis-
ease? Urology 1980;16(l):l-6.

10. Furlow WL: Therapy of impotence, in Clinical
Neuro-Urology, Krane RJ, Siroky MB (eds). Bos-
ton, Little Brown and Co, 1979, 213-228.

11. Scott FB, Byrd GI, Karacan I: Erectile impotence
treated with an inflatable penile prosthesis: Five
years of clinical experience. JAMA
1979;241(24):2609-2612.

Dr Baum is a urologist affiliated with Touro Infirmary in New Orleans.

Reprint requests should be sent to Dr Baum at 3525 Prytania St,
Suite 614, New Orleans, LA 70115.

50 JOURNAL VOL 140 JUNE

REPORTING AIDS CASES IN LOUISIANA

WHO SHOULD REPORT?

Every physician is required by law to report any case or suspected case of AIDS which he or she is attending,
has examined, or has prescribed for (Louisiana Sanitary Code, Chapter II, §2:004).

WHAT SHOULD BE REPORTED?

WHEN SHOULD I REPORT?

The report should be made promptly at the time the physician first visits, examines or prescribes for the
patient (Louisiana Sanitary Code, Chapter II, §2:004).

WHERE SHOULD I REPORT?

A diagnosed or suspected case of AIDS should be reported directly to the Epidemiology Section in New
Orleans.

By phone: (504) 568-5005

By mail: La. Office of Preventative and Public Health Services
Epidemiology Section
PO Box 60630
Room 615

New Orleans, LA 70160

WHY REPORT AIDS CASES?

CONFIDENTIALITY CONCERNS

All reports are kept absolutely confidential. Names of patients, physicians or hospitals are not released under
any circumstances.

JOURNAL VOL 140 JUNE 53

CALENDAR

JL, JBk Jrnmmm MLmm «JL ^1 WLmt!^ JIL, «mL JHw

July

July 1-5

2nd Annual Family Practice Board Review, San Diego. Con-
tact: Office of Continuing Medical Education, UC San Diego School
of Medicine, M-017, La Jolla, CA 92093; (619)534-3940.

July 6-13

Breast Imaging and Ultrasound, Alaska 88: Cruise the In-
land Passage. Contact: Medical Seminars International Inc, 21915
Roscoe Blvd, Suite 222, Canoga Park, CA 91304; (818)719-7380.

July 14-16

4th Annual Berkshire Medical Conference: Advances in Car-
diology, Hancock, Massachusetts. Contact: Berkshire AHEC,
(413)447-2417.

July 16-18

Laboratory and Clinical Aspects of Microbiological
Diagnosis, Newport Beach, California. Contact: Sydney M.
Finegold, MD, Dept of Continuing Education in Health Sciences,
Room 614, UCLA Extension, 10995 Le Conte Ave, Los Angeles,
CA 90024; (213)825-7257.

July 17-22

13th Annual National Wellness Conference, Stevens Point,
Wisconsin. Contact: National Wellness Institute, South Hall,
University of Wisconsin, Stevens Point, WI 54481; (715)346-2172.

July 19-23

Louisiana Academy of Family Physicians Annual Scientific
Assembly, Sandestin Beach Hilton, Destin, Florida. Contact:
LAPP, 4705 Iberville St, New Orleans, LA 70119.

July 21 - August 2

Italy and the Swiss Alps, Sponsored by INTRAV and the
Louisiana State Medical Society. Contact: Anita Bums, LSMS,
1700 Josephine St, New Orleans, LA 70113; (504)561-1033,
(800)462-9508.

July 24-28

34th Annual Southern OB-GYN Seminar, Asheville, North
Carolina. Contact: Dr. George Schneider, Ochsner Clinic, Dept

54 JOURNAL VOL 140 JUNE

of OB-GYN, 1514 Jefferson Hwy, New Orleans, LA 70121;
(504)838-4031.

July 24-29

8th Annual Internal Medicine Review, Hilton Resort, South
Padre Island, Texas. Contact: Scott & White Continuing Medical
Education Office, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

July 25-29

Sports Medicine 1988: A Practical Approach to Caring for
Today's Athlete, San Diego. Contact: Office of Continuing
Medical Education, UC San Diego School of Medicine, M-017, Im
J olla, CA 92093-0617; (619)534-3940.

August

August 13-14

Anesthesia for the Cardiac Patient Having Non-Cardiac
Surgery, San Diego. Contact: American Society of Anesthe-
siologists, 515 Busse Hwy, Park Ridge, IL 60068.

Discussions of Current Hand Care Concepts, San Diego.
Contact: Plastic Surgery Educational Foundation, 444 East Algon-
quin Rd, Arlington Heights, IL 60005; (312)228-9900.

August 14-19

Wilderness Medicine, Snowmass, Colorado. Contact: Office
of Continuing Medical Education, UC San Diego School of
Medicine, M-017, La Jolla, CA 92093-0617; (619)534-3940.

August 21-30

INTRAV Cruise on the Queen Elizabeth 2 and London, Con-
tact: Anita Bums, Louisiana State Medical Society, 1700 Josephine
St, New Orleans, LA 70113; (504)561-1033, (800)462-9508.

August 27

Teleplast Teleconference on Fasciocutaneous Flaps,

Metairie, Shreveport, and Baton Rouge, Louisiana. Contact:
Plastic Surgery Educational Foundation, 444 East Algonquin Rd,
Arlington Heights, IL 60005; (312)228-9900.

September

September 6-9

3rd Annual Plastic Surgery of the Breast Symposium, San-
ta Fe, New Mexico. Contact: Plastic Surgery Educational Foun-
dation, 444 East Algonquin Rd, Arlington Heights, IL 60005;
(312)228-9900.

September 10-18

September 14-19

Cosmetic Surgery of the Face and Breast, Monte Carlo,
Monaco. Contact: Francine Leinhardt, Conference Coordinator,
210 East 64th St, New York, NY 10021; (212)838-9200 ext 2776.

September 17-18

Metropolitan Regional Refresher Course, Las Vegas. Con-
tact: American Society of Anesthesiologists, 515 Busse Hwy, Park
Ridge, IL 60068.

September 17-19

4th Aimual Meeting of the American Society for Reconstruc-
tive Microsurgery, Baltimore. Contact: ASRM, 3025 South
Parker Rd, Suite 65, Aurora, CA 80014.

October

October 3-5

NIH Consensus Development Conference: Urinary Incon-
tinence in Adults, Bethesda, Maryland. Contact: Conference
Registrar, Prospect Associates, Suite 500, 1801 Rockville Pike,
Rockville, MD 20852; (30D468-MEET.

October 3-7

6th Annual Comprehensive Review of Vascular Surgery,

Santa Monica, C^ornia. Contact: UCLA Extension, PO Box
24901, Los Angeles, CA 90024-0901; (213)825-1901.

October 8-12

American Society of Anesthesiologists Annual Meeting, San

Francisco. Contact: ASA, 515 Busse Hwy, Park Ridge, IL 60068.

October 8-15

10th International Seminar on Operative Arthroscopy,

Kauai, Hawaii. Contact: UCLA Extension, Dept of Continuing
Education, PO Box 24901, Los Angeles, CA 90024-0901;
(213)825-1901.

October 8-16

13th Aimual International Body Imaging Conference, Maui,
Hawaii. Contact: Annual Body Imaging Conference, 21915 Roscoe
Blvd, Suite 222, Canoga Park, CA 91304; (818)700-9821.

October 12-14

Hip and Knee Reconstructive Surgery 1988, Kauai, Hawaii.
Contact: UCLA Extension, Health Sciences Dept, PO Box 24901,
Los Angeles, CA 90024-0901; (213)825-1901.

November

November 2-5

Optimizing Management of Primary Bone Tumors: An In-
ternational Symposium Emphasizing the Multidisciplinary
Approach, Houston. Office of Conference Services, M. D. Ander-
son Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030;
(713)792-2222.

November 5

Teleplast Teleconference on Management of Craniomax-
illofacial Trauma, Metairie, Shreveport, Baton Rouge, Louis-
iana. Contact: Plastic Surgery Educational Foundation, 444 East
Algonquin Rd, Arlington Heights, IL 60005; (312)228-9900.

November 10-13

Lasers for the Plastic Surgeon, Orlando, Florida. Contact:
Plastic Surgery Educational Foundation, 444 East Algonquin Rd,
Arlington, Heights, IL 60005; (312)228-9900.

November 11-12

Advances in the Treatment of Pediatric Bones: Craniofacial,
Orthopedic, Neurosurgical, Dallas. Contact: Linda Henry,
Humana Hospital - Medical City Dallas, 7777 Forest Lane, Dallas,
TX 75230; (214)661-7000.

November 17-20

Assuring the Future Fiscal Survival of Consultation —
Liaison Psychiatry and Psychosomatic Medicine, New

Orleans. Contact: Academy of Psychosomatic Medicine, 5824 N
Magnolia, Chicago, IL 60660; (312)784-2025.

JOURNAL VOL 140 JUNE 55

PROFESSIONAL LISTINGS

THE FERTILITY INSTITUTE OF NEW ORLEANS

(A Professional Corporation)

Richard P. Dickey, MD, PhD

Diplomate, American Board of
Reproductive Medicine
Diplomate, American Board of
Obstetrics and Gynecology

Steven N. Taylor, MD

Diplomate, American Board of
Obstetrics and Gynecology

David N. Curole, MD Phillip H. Rye, MD

Diplomate, American Board Diplomate, American Board

of Obstetrics and Gynecology of Obstetrics and Gynecology

Terry Olar, PhD

Director, InVitro Laboratory
Member, Society for the
Study of Reproduction

REFERRALS ACCEPTED FOR IN VITRO FERTILIZATION
AND OTHER INFERTILITY THERAPY INCLUDING;

MAIN OFFICE

SLIDELL OFFICE

UPTOWN OFFICE

6020 Bullard Ave
New Orleans, LA 70128
(504) 246-8971
(504) 246-8795

700 Cause Blvd
Suite 101
SlideU, LA 70458

2633 Napoleon Ave
Suite 805

New Orleans, LA 70115

TOURO INFIRMARY'S CENTER FOR CHRONIC PAIN

AND

DISABILITY REHABILITATION

1401 Foucher St
New Orleans, LA 70115
(504) 897-8404

Richard H. Morse, MD

Medical Director

Jackie Chauvet

Liaison Coordinator

Elizabeth Messina, RN

Unit Supervisor

56 JOURNAL VOL 140 JUNE

JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY July 1988

STACKS

- ^

The five horsemen of rheumatology

ALSO

KAWASAKI'S SYNDROME ACCOMPANIED
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A COMMITMENT TO SERVE THE LOUISIANA PHYSICIAN

EDITOR

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Ex officio, DANIEL H. JOHNSON JR, MD

EDITORIAL BOARD

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EXECUTIVE COMMITTEE

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R. BRUCE WILLIAMS, MD
HOWARD A. NELSON JR, MD
RONALD J. FRENCH, MD
FRANK J. GEORGE, MD
PHILIP A. ROBICHAUX JR, MD
JAMES R. BERGERON, MD
DAVID M. WALSWORTH, MD
CHARLES D. BELLE AU, MD
G. MICHAEL KENT, MD
LEO L. LOWENTRITT JR, MD
EMILE K. VENTRE JR, MD
STANFORD A. OWEN, MD
WALLACE H. DUNLAP, MD

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JOURNAL

"" OF THE LOUISIANA STATE MEDICAL SOCIETY

1988

VOLUME 140 / NUMBER 7 /

JULY

ARTICLES

Jack Waxman, MD

The five horsemen of
rheumatology

Irwin Cohen, MD
Michael Whistler, MD

Kawasaki's syndrome
accompanied by bone
marrow suppression

Joan H. Wightkin, MPH
Linda M. Lambert, MPH

Cesarean childbirth rate
among women in the
New Orleans area

DEPARTMENTS

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Viewpoint

ECG of the Month

Books Received

Otolaryngology/Head
& Neck Surgery Report

Auxiliary Report

" Calendar

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ASSISTANCE WITH YOUR ELDERLY PATIENT LOAD:

CASE EXAMPLE

IT WILL COME as no surprise to the
I practicing physician that a
[growing percentage of the patient
load is elderly. The increasing age
of the patient load brings with it a
set of problems that did not exist
when the physician was in train-
ling. Health care needs of the el-
derly population are changing:
acute care needs no longer domi-
nate; chronic diseases account for
the top ten disease states in the el-
derly population.^

These chronic disease states
require more than just medical in-
tervention. Due to the long term
course of treatment, they necessi-
tate involving community re-
sources and family counseling. The
treatment is not only for the dis-
ease but also for the ongoing con-
sequences of the disease.^

CASE REPORT

A 66-year-old white woman was
brought to the Louisiana Geriatric
Assessment Center by her son,
who wanted to have his mother in-
terdicted with himself as curator,
due to her long term alcohol and
drug abuse. The son had legal
guardianship in Florida but was
moving his mother to be near him
in Louisiana. The patient had a di-
agnosis of dementia secondary to

her alcohol abuse. She had re-
ceived psychotherapy and halo-
peridol (Haldol®) in Florida with
no improvement. She had had an
oophorectomy in the distant past
for an unknown cause. There were
no known allergies. Medications at
time of visit included Haldol® 5
mg three times daily and benztro-
pin mesylate (Cojentin®) 5 mg
twice a day.

The patient had also been
evaluated by the Minnesota Mul-
tiphasic Personality Inventory In-
terpretive System and had been di-
agnosed as having had a psychotic
episode. She had some alteration
in thought processes with regard
to auditory hallucinations and de-
lusional thinking for which she had
received treatment in Florida.

While in Florida, she had lived
alone. Her closest relatives were in
Louisiana. Family and social his-
tories were not remarkable.

On examination, the patient
was pleasant and appeared in no
distress. Physical findings were
unremarkable except for the men-
tal status examination that re-
vealed a decrease in overall mem-
ory, especially in short-term
memory. The psychosocial inter-
view revealed a woman who
wanted to return to Florida and
who very much wanted to main-

tain her independence and was
fearful of nursing home place-
ment. She engaged in a variety of
activities, including shopping.

The diagnosis after the initial
assessment agreed that she had
significant cognitive impairments.
The care plan's recommendations
were: to continue the present med-
ications, to immediately stop al-
cohol consumption, to seek a shel-
tered living environment with
supportive services and supervi-
sion, to engage in community ac-
tivities such as senior center activ-
ities, and to maintain the same legal
supervision that existed in Florida.
Care management services were
suggested to ease the implemen-
tation of these recommendations.
The patient and the family were
encouraged to monitor progress
after the move and to consider
reassessment, possibly a reversal
of the curatorship/guardianship, if
her functioning improved with
treatment.

Six months later, the son
phoned requesting a reassessment
of his mother. He thought that she
was doing much better and wanted
another opinion regarding her
functioning capacity. Upon reas-
sessment, it was found that she was
significantly improved, exhibited
no cognitive deficits, and had re- k

JOURNAL VOL 140 JULY 3

mained off alcohol. The patient and
her family had followed the care
plan with assistance of a care man-
ager. As a result of these findings,
her son decided to have the in-
terdiction reversed. His mother was
once again in full control of her life
legally as well as functionally.

DISCUSSION

The American College of Physi-
cians recently issued a position pa-
per on the use of comprehensive
functional assessment for elderly
patients. In summary they felt that
"functional assessment proce-
dures should be recognized as
identifiable, specific cognitive
services . . . that can be useful in
systematically assessing functional
deficits that otherwise might be
overlooked by conventional ex-
amination methods." The paper
goes on to say that clinical practice
should include the provision of "a
needed measure of functional out-
come, by comparing changes in
function over time as affected by
disease and other life events (such
as bereavement), and the subse-
quent management of these prob-
lems."^

In the above case the diagnosis
was easy and had already been
made. What had been missing in
the evaluation was a frank discus-
sion of the long term consequences
of the disease. As so often happens
with the elderly, it is the manage-
ment of these long term conse-
quences that is the most trouble-
some and costly. This case
demonstrates that careful assess-
ment and care planning which fo-
cus on diagnosis and its long-term
social, financial, and psychological
effects can benefit the patient and.

in the long run, save dollars. The
dollars Medicare provided for the
assessment were minimal com-
pared to the cost of long-term in-
stitutionalization .

These patients do need a pri-
mary care physician, but many
times this physician is called upon
not only to make medical diag-
noses and prescribe treatment but
to make legal decisions and to be
an information and referral center
for all supportive community serv-
ices.

The geriatric functional as-
sessment provides all of the above
on a consultative basis. The as-
sessment does not replace the pri-
mary physician but rather supplies
a team which assesses the patient's
physical needs in the broader con-
text of environment, family dy-
namics, and past social history. A
care plan is developed which de-
scribes both short-term and long-
term goals and includes commu-
nity resources, changes in living
arrangements, and other pertinent
information. This plan gives the
primary physician and the patient
a blue print for continued treat-
ment and guidance.

A related and supplementary
service is care management. In the
case of this patient, a care manager
stepped in and arranged the nec-
essary services: helping her with
housing decisions, facilitating her
participation in senior center activ-
ities, and monitoring her compli-
ance with the treatment regime.
Her family was free to enjoy her
presence and to continue the fi-
nancial management. They were
relieved of the burden of single-
handedly trying to implement the
care plan and of negotiating the red
tape of the community service de-

livery system. The physician was
free to continue with ongoing
treatment as necessary without
being expected to "fix" her world
and address her family's concerns.

Taken together, the geriatric
functional assessment process and
care management offer a complete
package of services to augment the
treatment a physician can offer.
They are commplementary serv-
ices to support medical care and
manage the chronic conditions so
prevalent among the elderly pop-
ulation. ■

REFERENCES

1. Aging America: Trends and Projections. US Dept
of Health and Human Services, 1985-86. US
Senate Special Committee on Aging, American
Association of Retired Persons, Federal Coun-
cil on Aging, Administration on Aging.

2. Rubenstein LZ, Campbell LJ, Kane RL: Clinics
In Geriatric Medicine: Geriatric Assessment, Vol
3(1). Philadelphia, WB Saunders Co, 1987.

3. Comprehensive Functional Assessment For Elderly
Patients. American College of Physicians, Jan-
uary 15, 1988.

TIMOTHY J. HOLT, MD
SARA S. HUNT, MSW
MADELINE MONROE, RN
ROSE COLLEY, MSW

4 JOURNAL VOL 140 JULY

ECG OF THE MONTH

CAREFUL NEGLECT

JORGE I. MARTINEZ-LOPEZ, MD

The tracing shown below belongs to a 71-year-old man hospitalized with acute onset of severe
retrosternal chest pain. The continuous rhythm strip was recorded before therapy was begun.

What is your diagnosis? Elucidation is on page 8.

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JOURNAL VOL 140 JULY 7

ECG of the Month.

Case presentation is on page 7.

DIAGNOSIS — Acute inferior wall myocardial infarction
and intermittent bundle branch block

Sinus tachycardia, at a rate of 107 times a minute, is
present.

The interesting feature on the rhythm strip is
that, although sinus rhythm is present throughout its
length, there are two different QRS morphologies.
These morphologies and their responsible mechan-
isms are the subject of the discussion to follow.

DISCUSSION

Two types of QRS complexes are identified on the
rhythm strip: a QRS complex of normal duration; a
wide QRS complex with a duration of 0.12 sec.

To facilitate analysis of the rhythm strip, let us
first examine the narrow QRS complexes. They meas-
ure 0.08 sec in duration and are preceded by sinus P
waves with normal PR intervals. These findings in-
dicate that the narrow QRS complexes occur in re-
sponse to the prevailing sinus rhythm and that con-
duction into the ventricles is normal. Prominent in
the narrow QRS complexes are Q waves and elevated
ST segments that are consistent with the ECG diag-
nosis of acute inferior wall myocardial infarction. Acute
inferior wall myocardial infarction is most often the
result of compromised circulation in the right coro-
nary artery; less often, the left circumflex coronary
artery is the vessel involved. In either case, the most
common conduction abnormality is at the AV junc-
tional level beause the AV nodal artery comes off the
vessel irrigating the inferior wall of the left ventricle.

Let us now turn our attention to the wide QRS
complexes. The sequence that begins after the fourth
narrow QRS on the top panel starts and ends with a
wide QRS that is premature, relative to the preceding
cycle, and does not have a sinus P in front of it. The
intervening wide QRS complexes of that sequence
recur regularly and are preceded by sinus Ps. Towards
the end of the third panel, a brief sequence of wide
QRS complexes starts and ends abruptly, without a
premature wide QRS. Lastly, in the bottom panel, the
three-beat wide QRS sequence with Ps in front end
with a fourth wide QRS that is premature. Five nar-
row QRS complexes later, a premature wide QRS oc-

curs alone.

The train of events described above raise ques-
tions relative to the mechanisms responsible for the
wide QRS complexes. Do they present supraventric-
ular premature complexes conducted downgrade with
aberration, accelerated idioventricular rhythm, or in-
termittent bundle branch block?

The possibility that all of the wide QRS complexes
represent aberrant ventricular conduction of prema-
ture supraventricular impulses can be dismissed
quickly. Although premature wide QRS complexes
are recorded at the beginning and end of one se-
quence, at the end of another, and as an isolated event
(bottom panel), it is clear that all the other wide QRS
complexes are preceded by sinus Ps with a fixed PR
interval.

Similarly, accelerated idioventricular rhythm
(AIVR) is an unlikely mechanism responsible for the
wide QRS complexes. AIVR, a relatively common ar-
rhythmia in acute myocardial infarction, is a ventric-
ular escape rhythm. Therefore, its emergence is
marked by slowing of the sinus rhythm, with and
without intervening “fusion beats." Because AIVR is
an escape rhythm, AV dissociation by default is also i
present. In the tracing shown here, sinus Ps have a
constant relationship with the wide QRS complexes
that follow them.

The third option, intermittent bundle branch
block, is the most plausible. The majority of instances
of intermittent bundle branch block are due to changes
in cycle length — even when minimal. This electro-
physiological phenomenon is termed rate-related or
rate-dependent bundle branch block. In such cases, ap-
pearance of the bundle branch block patterns may
occur when the cardiac cycle length either narrows
(tachycardia-dependent block) or lengthens (brady-
cardia-dependent block). On occasion, tachycardia-
and bradycardia-dependent block coexist.

The mechanisms responsible for the develop- i
ment of rate-dependent block have yet to be clarified.

It has been postulated that in tachycardia-dependent
block, repolarization is prolonged, whereas the bra-
dycardia-dependent block is related to hypopolari-
zation and reduction in membrane responsiveness.
Similar mechanisms have been proposed for rate-de- !
pendent blocks observed in myocardial ischemia. As
myocardial ischemia becomes less, intraventricular
conduction improves.

In the present case, the evolving myocardial in-

8 JOURNAL VOL 140 JULY

1 ,

farction played a major role in predisposing the pa-
tient to rate-dependent block. The phenomenon was
transient and disappeared after the myocardial in-
farction was completed. During evolution of the my-
ocardial infarction, minimal lengthening of the PP in-
terval appeared to be responsible for the rate-
dependent block when it appeared abruptly. Minimal
changes in cycle length may not be clearly obvious
when tracings are recorded at the conventional speed
(25mm/sec), but may become obvious at a paper speed
of lOOmm/sec. In other portions of the tracing, supra-
ventricular premature impulses conducted aberrantly
into the ventricles set the stage for initiation and/or
termination of the rate-dependent block. In the bot-
tom panel, however, the isolated, premature supra-
ventricular impulse conducted with aberration failed
to trigger what others did.

Rate-dependent block, in itself, is benign, and
does not require medical or electrical therapy, only
"careful neglect." In other words, while ECG moni-
toring and awareness of the presence of rate-depend-
ent block are important, intervention is not necessary.
Bradycardia-dependent bilateral bundle branch block
deserves special attention, as it may result in parox-
ysmal AV block and hemodynamic alterations.

A final word. In this patient, the development of
the bundle branch block pattern masked the ECG
findings of acute, evolving, inferior wall myocardial
infarction. ■

SELECTED REFERENCES

1. El-Sherif N: Tachycardia-dependent versus bradycardia-dependent inter-
mittent bundle branch block. Br Heart J 1972;34:167-176.

2. Rosenbaum MG, Elizari MV, et al: The mechanism of intermittent bundle
branch block. Relationship to prolonged recovery, hypopolarization and
spontaneous diastolic depolarization. Chest 1973;63:666-667.

3. El-Sherif N: Tachycardia- and bradycardia-dependent bimdle branch block
after acute myocardial ischemia. Br Heart J 1974;36:291-301.

4. El-Sherif N, Scherlag BJ, Lazzara R: Bradycardia-dependent conduction
disorders. J Electrocardiol 1976;9:1-4.

5. Mitamura H, Ogawa S, et al: A case of coexisting tachycardia- and bra-
dycardia-dependent bilateral bundle branch block. / Electrocardiol
1981;14:195-200.

Health Care
^ Marketing
As PersonaiAs
• ^Your Bedside Manner

f As 2i physician you understand the need
for personal attention.

Call for details, or complete the reply card in this
publication and mail today.

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BOOKS RECEIVED:

The JOURNAL seeks reviews of the following books. Interested
physicians should contact f/re JOURNAL, 1700 Josephine St, Nezv
Orleans, LA 70113; (504) 561-1033, (800) 462-9508.

INFORMED CONSENT: A Survival Guide

Donald J. Palmisano, MD, JD, Hebert J. Mang Jr, JD; New

Orleans, Invictus Publishing Co, 1987, 47 pages.

TO BE OR NOT TO BE HUMAN: The Traits of Human Nature
Ben Freedman, MD; New York, Vantage Press, 1987, 509
pages.

Dr Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, TX.

The opinions and assertions contained herein are the private views of the
author and not to be construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

JOURNAL VOL 140 JULY 9

FOR A FREE BROCHURE CALL THE DIRECTOR OF ADMISSIONS -(601) 467-9057.

St Stanislaiis
helps build leadeiis.

J ames E. Smith graduated
from St. Stanislaus in 1945.

He went on to serve as presi-
dent of T. Smith & Son, Inc.
of New Orleans as well as the Dock Board.

“The sense of moral values instilled in me at
St. Stanislaus has been the cornerstone of my

whole adult life!’

BOARDING SCHOOL GRADES 6-12
SUMMER CAMP AGES 9-14

304 South Beach Blvd. Bay St. Louis, MS 39520

To the Brothers of the Sacred Heart, every
student is a potential leader. And giving him
the proper example— spiritual, intellectual
and moral — is our mission at St. Stanislaus.

SAIIMT STVXrJISLALJS

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

MENIERE’S DISEASE:

REVIEW AND UPDATE

LORNA BRASS, MD; PAUL A. BLAIR, MD

This is a brief review of the clinical findings,
pathology, and present concepts in the etiology of
Meniere's disease. There is a discussion of
evaluation and multiple modes of therapy.

M eniere's Disease is a disease affecting the inner
ear. The hallmark of the disease is the triad of
symptoms: vertigo, tinnitus, and fluctuating hearing
loss.^ In addition, a sensation of fullness in the ear is
common. The disease has been reported in children
(Hausler, et al) but usually occurs after 20 years of
age and rarely after 60.^ Although the incidence is not
precisely known, there are approximately 100,000 new
cases per year and about 2.4 million people affected
in the United States. The disease is usually unilateral
but up to 20-30% of patients will eventually have in-
volvement of the other ear. This appears to be more
likely in individuals whose onset of Meniere's disease
is later in life. Patients usually have most or all of the
classic findings but, occasionally, one symptom pre-
dominates or precedes the others.

The disease was first described by a French phy-
sician, Prosper Meniere, in 1861. It was not until 1938
that a probable histopathology was known. Hallpike
and Cairns in England, as well as Yamakawa in Japan,
noted hydropic distention of the endolymphatic sys-
tem.^ Despite much research, the pathogenesis of
Meniere's disease remains unknown.

JOURNAL VOL 140 JULY 11

CLINICAL FINDINGS

Vertigo

This is the most distressing and disabling of the symp-
toms and the most likely to cause the patient to seek
medical attention. The pattern of these episodes can
be quite variable. They may last from 20 minutes to
several hours with normal equilibrium between epi-
sodes. They may occur with greater and greater fre-
quency as the disease progresses and then begin to
decrease, or they may occur in clusters with long pe-
riods free of vertiginous episodes. The episodes may
be preceded by a sensation of aural fullness or a greater
decrease in hearing and may be accompanied by nau-
sea and vomiting, prostration, diaphoresis, and pal-
lor. Although the "spell" may have preliminary
symptoms, this aura is never accompanied by sei-
zures, loss of consciousness, paralysis, or dysarthria.
As the episode abates (which may take hours), the
patient may fall asleep and upon awakening feel to-
tally normal. There is no postictal phase. There may
be some motion intolerance that lasts several days.
Hearing on the affected side may remain decreased
after the episode but is occasionally found to improve,
a paradoxical improvement called Lermoyez's syn-
drome.

Two other patterns of vertiginous spells also oc-
cur. The first, lasting only a few seconds, usually
brought on by sudden movement, consisting of a mo-
mentary loss of balance, gives the appearance of an
inebriated gait. The second type of spell dubbed
"fainting spells of Tumerkin" or "Utricular crises" are
short, severe episodes of vertigo that occur without
aura or warning. The patient is thrown violently to
the ground. Again, there is no loss of consciousness
and these drop attacks are usually brief.

The vertigo of Meniere's disease is of the periph-
eral type. As with all true vertigo there is a sense of
movement either of the patient, or of his surround-
ings. This peripheral vertigo is characterized by sud-
den onset, short duration, paroxysmal nature, intense
severity, exacerbation by position or movement often
with a latency, and fatiguability if the sensation is
always in the same direction. It may be accompanied
by horizontal nystagmus, shifting from toward the
side of the lesion early in the disease process, to away
from the lesion side later in the course. Other otologic
symptoms, such as tinnitus and hearing loss as well

12 JOURNAL VOL 140 JULY

as systemic symptoms of nausea and vomiting may
occur with peripheral vertigo. Peripheral vertigo is an
indication of a lesion in the semicircular canals or
vestibular nerve. In contradistinction, central vertigo
is an indication of a lesion of the vestibular nuclei,
the vestibular tracts in the brain stem, the cerebellum,
or the cerebrum. Central vertigo is characterized by
slow onset lasting days to months, by a more contin-
uous state, and by less severity. Nystagmus may be
horizontal, rotary, or vertical without accompanying
otologic or systemic symptoms but possibly accom-
panied by other neurologic symptoms.

Tinnitus

Tinnitus of Meniere's disease may be episodic or con-
tinuous. It does not have a pulsatile nature nor does
it change with change in carotid pressure. The pitch
tends to parallel the area of hearing loss; the pitch of
the tinnitus is low if the hearing loss is in the low
frequencies.

Hearing Loss

Auditory acuity changes in Meniere's disease are of
the sensorineural type typical of cochlear damage. An
acute decrease in auditory acuity almost always ac-
companies attacks of vertigo. The loss is fluctuating
and may not be detected at the early stages of the
disease. If the disease continues, these fluctuations
in hearing become less obvious and are replaced by
a steady decrease in acuity. Hyperacusis is usually
present secondary to recruitment. In addition, the
same pitch may be perceived as two different pitches
by the two ears, known as diplacusis binauralis dys-
harmonica and is usually higher in perceived pitch in
the affected ear.

Aural Fullness

This disturbing symptom occurs in most patients with
Meniere's disease. It may intensify preceding a ver-
tiginous episode but is usually constant. This symp-
tom may be the first symptom noticed in the pro-
gression of the disease.

ETIOLOGY

Although the relationship between endolymphatic
hydrops and Meniere's disease is well established,
the cause of this disturbance in labyrinthine fluids is
not known. Increase in endolymphatic pressure could
be secondary to over-production or under-resorption

of the fluid. Research has been done to evaluate pos-
sible mechanical obstruction of the endolymphatic duct
or the vestibular aqueduct, or possible endolymphatic
sac abnormality. Electrolyte disorders have been im-
plicated with specific attention to potassium and cal-
cium abnormalities.^'^ Endocrine abnormalities in-
cluding hyperthyroidism, pancreatic insufficiency and
decreased adrenal function have been reported in
Meniere's patients to a greater degree than in the
general population. Vascular disease in the form of
arterial insufficiency, anatomic abnormalities, or ve-
nous congestion have been proposed as factors in
endolymphatic hydrops.^' ^ Autoimmune disease has
been implicated with type II reaction, coUagen anti-
gen-antibody complexes being the cause of initial
damage.® Evidence of increased circulatory complexes
have been reported by some researchers but refuted
by others. XeneUis found a correlation with one hu-
man lymphocyte antigen group but other evidence of
autoimmune disease was lacking.^

AUergy has been implicated in a small percentage
of Meniere's patients (Stable). The proposed mech-
anism was not type I antigen-antibody mediated but
rather an alternate definition described by Rinkle,
Bryant, and others.

Finally, certain dependent personality types are
said to be more prone toward Meniere's disease.

With etiology stiH unclear but pathophysiology
accepted most therapies are based on correction of
the pressure shift in the labyrinth and palliation of
symptoms.

PATHOLOGY

Endolymphatic hydrops, the main pathologic finding
in Meniere's disease, can be described as swelling of
the endolymph containing structures. This may lead
to shift in the central structures of the cochlea.

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of fistulas between the endolymph and perilymph
filled spaces. These distortions ultimately lead to dys-
function of the cochlea. There is a loss of cochlear
elements only occasionally; hair cells and ganglion
cells are usually normal in histology and number.

PHYSICAL EXAMINATION AND
FUNCTIONAL TESTING

Very often, there are no unusual findings and the
general physical, neurological, and otologic exami-
nations are within normal limits.

Vestibular Tests

If the patient is tested during an acute vertiginous
episode nystagmus is always present. Electronystag-
mogram will usually demonstrate nystagmus with the
eyes closed for several days after an episode. The most
common finding is hypoactivity of the involved lab-
yrinth to caloric testing. This testing may also precip-
itate symptoms. NadoP^ found an abnormal fistula
test in 30% of patients with Meniere's disease and this
group of patients appeared more reactive to negative
pressure than to positive pressure.

Audiography

Pure tone audiograms classically show a low fre-
quency sensorineural hearing loss, but progression of
the hearing loss may show a flat loss throughout the
frequency range. Occasionally upward sloping hear-
ing loss is seen.

Discrimination scores are variable but are usually
in the range appropriate to the pure tone losses dem-
onstrated.

Glycerol Test

Glycerol administered to the patient acts as a diuretic.
The pure tone audiogram is checked before and 3
hours after administration. Serum osmolality is also
checked to make sure a diuretic effect is achieved.
Since diuresis theoretically causes a shift in the coch-
lear fluid and thus a temporary relief of the endo-
lympthatic hydrops, an improvement in the audi-
ogram is considered diagnostic of Meniere's disease;
although negative results do not rule out the diag-
nosis. This test must be administered fairly early in
the course of the disease.

Electrocochleography

While not used at most centers, electrocochleography
14 JOURNAL VOL 140 JULY

TABLE 1

CLASSIFICATION OF EFFICACY OF VARIOUS THERAPIES
FOR MENIERE’S DISEASE

Class

Results

Absence of definitive vertiginous spells for
the described period
Hearing improved.

Absence of definitive vertiginous spells for
the described period
Hearing unchanged.

Absence of definitive vertiginous spells for
the described period
Hearing worse.

Failure to control definitive spells.

has been proposed as a means to select patients who
may go on to develop bilateral disease. Coats and
Kidder^^ found 68% of patients with Meniere's disease
had an abnormal electrochochleogram and Coin, et
aP^ had similar results, reporting 62% of Meniere's
patients had an abnormal study.

Auditory Brainstem Response

Since the presenting symptoms and audiogram may
not be discriminating enough to separate Meniere's
disease from retrocochlear disease such as acoustic
neuroma, auditory brainstem response is the screen-
ing test of choice to separate these entities.

THERAPY

Treatment of Meniere's disease is designed to either
alter the course of the disease or ameliorate the symp-
toms. Various committees of the American Academy
of Ophthalmology and Otolaryngology have estab-
lished a scoring system to compare the efficacy of
different modalities of therapy (Table 1).

Medical Therapy

In the course of an acute vertiginous attack, control
of symptoms is usually affected using sedatives, an-
tiemetics, and vestibular suppressants, along with bed
rest and appropriate fluids.

One of the earliest therapies attempted in the
treatment of the vertigo of Meniere's disease was ha-
bituation.^^ Although there is a physiologic basis for
this treatment, the episodic nature of Meniere's ver-
tigo is poorly responsive to the fatigue effects applied

to the vestibular system. Thiazide diuretics with po-
tassium supplement have long been regarded as the
best initial therapy. Some author's have advocated
including a low salt diet.

Streptomycin as discussed by Moretz/® has been
used as a vestibular ablative agent in patients with
I bilateral disease, where preservation of hearing is
1 needed.

j Local infusion of aminoglycosides into the laby-
j rinth has also been advocated by Beck.^^

Other medical therapies are directed at specific
! causes. Allergy therapy and immune therapy have
been tested but thus far have not proved particularly
I effective. None of the medical therapies has appeared
to alter the natural course of the disease.

; Surgical Therapy

Surgical intervention has the potential to prevent or
I reduce progressive labyrinthine destruction. Patient
I selection is difficult since some patients will have a

spontaneous remission or respond to medical ther-
apy.

Choice of operation is also difficult. Kitahara^°
reports on 18 years of experience with an endolym-
phatic sac mastoid shunt. A total of 78% of patients
who underwent the procedure received class A re-
sults. Hearing was worsened in only 15% of patients.
For those undergoing endolymphatic sac-subarach-
noid shunt 45-50% showed class A or B results and
30-40% showed class D results at the end of 5 years.
Smyth^ reports 73% A or B results after vestibular
nerve section compared to 5% class D results with 6-
to 56-month foUow-up. Comparing vestibular nerve
section to saccus decompression. Primrose^ found the
former to be far superior for permanent relief of ver-
tigo. Similarly, Boyce^^ reports relief of vertigo in 96%
of patients who underwent retrolabyrinthine vesti-
bular nerve resection. Labyrinthectomy is still done
in cases of intractable vertigo if there is no auditory
activity left in the ear. There are other assorted pro-

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cedures including cryosurgery, ultrasound, trans-
stapedial tack placement, and osmotic induction of
the round window, but these methods have generally
fallen out of favor.

Complication rates for most of these procedures
are fairly low in experienced hands and are similar to
those in patients undergoing mastoidectomy.

SUMMARY

Meniere's disease is a process of variable clinical be-
havior, with spontaneous remissions or steady down-
hill course, of single episode or longstanding dura-
tion.

The etiology of this disease remains elusive. The
body of knowledge continues to grow concerning
possible causes and contributing factors.

Effective therapy can be rendered for many pa-
tients if a continuum from conservative medical ther-
apy to radical surgery is considered with the goal of
relief of distressing symptoms and conservation of
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REFERENCES

1. Paparella MM, Shumrick DA: Otolaryngology. New York, AB Saunders,
1980, pp 1878-1888.

2. Hausler R, Toupet M, Guidetti G, et al. Meniere's disease in children.
Am J Otolaryngol 1987;8(4):187-193.

3. Hallpike C, Cairns SH: Observation on the pathology of Meniere's dis-
ease. / Laryngol 1938;53:625.

4. Meyer zum Gottesberge AM, Ninoyu O: A new concept in pathogenesis
of experimental hydrops: Role of calcium. Aviat Spac Environ Med
1987;58(9):A240-246.

5. Kanazuki KE: Vascular loops in auditory canal as possible cause of Me-
niere's disease auris nasus Laryngoscope 1986;3(2):5105-5111.

6. Fukzawa T, Ohmura MY: The effect of injection of high K-l- solution
into scala media. Acta Otolaryngol (Stockh) 1987;103(3-4):170-175.

7. Gussan R: Vascular mechanisms in Meniere's disease: Theoretical con-
siderations. Arch Otolaryngol 1982;108:544-546.

8. Yoo TJ: Etiopathogenesis of Meniere's disease: A hypothesis. Ann Otol
Rhinol Laryngol 1984;113 (Suppl):6-12.

9. Xenellis J, Morrison AW, McClowskey D, et al. HLA antigens in the
pathogenesis of Meniere's disease. / Laryngol Otol 1986;100(1):2104.

10. Stable J, et al: Meniere's disease and allergy with special references to
immunoglobulin and IgE antibody (regin) in serum. Equil Res 1974;4:22-
27.

11. Wexler M, Crary WG: Meniere's disease: The psychosomatic hypothesis.
Am J Otol 1986;7(2):93-96.

12. Nadol JB: Positive Hennebert's sign in Meniere's disease. Arch Otolar-
yngol 1977;103:524-530.

13. Skalabrin TA, Margham CA: Analysis of the glycerin test for Merviere's
disease. Otolaryngol Head Neck Surg 1987;96(3):282-288.

14. Coats A, Kidder H: The summating potential and Meniere's disease: I
Summating potential amplitude in Meniere's and non-Meniere's ears.
Arch Otolaryngol Head Neck Surg 1981;107:199-208.

15. Goin D, Stoller S, Asether D, et al: Summating potential in Meniere's
disease. Laryngoscope 1982;92:1383-1389.

16. Norr ME, DeWeerdt W: Treatment of vertigo based on habituation. Phy-
sio-pathological basis. / Laryngol Oto 1980;94(7):689-96.

17. Van Deelen GW, Huizing EH: Use of diuretic (Dyazide®) in the treat-
ment of Meruere's disease. A double blind cross-over placebo controlled
study. ORL ] Otorhinolaryngol Relat Spec 1986;48(5):281-292.

18. Moretz WH Jr, Shea JJ Jr, Orchik DJ, et al: Streptomycin treatment in
Meniere's disease. Otolaryngol Head Neck Surg 1987;96(3):256-259.

19. Beck C: Intratympanic application of gentamydn for treatment of Me-
niere's disease. Keio } Med 1986;35(1):36-41.

20. Kitahara M, Katajima K, Yazawa Y, et al: Endolymphatic sac surgery
for Meniere's disease: Eighteen years experience with the Kitahara sac
operation. Am J Otol 1987;8(4):283-286.

21. Brackman DE, Nissen RL: Meniere's disease. Results of treatment with
endolymphatic subarachnoid shunt compared with endoylmphatic mas-
toid shunt. Am J Otol 1987;8(4):275-282.

22. Smyth GD, Kerr AG, Gordon DS, et al: Vestibular nerve section for
Meniere's disease. J Laryngol Otol 1976;80:823-831.

23. Primrose WJ, Smyth GD, Kerr AG, et al: Vestibular nerve section and
saccus decompression: An evaluation of long term results. / Laryngol Otol
1986;100(7)775-784.

24. Boyce SE, Mischke RE, Goin DW: Hearing results and control of vertigo
after retrolabyrinthine vestibular nerve section. Laryngoscope 1988;8(3):257-
261.

Dr Brass is a resident in the Dept of Otolaryngology — Head and Neck
Surgery at Tulane University Medical Center in New Orleans.

Dr Blair is otolaryngologist and facial plastic surgeon in New Orleans.
He is also a professor in the Dept of Otolaryngology — Head and Neck
Surgery at Tulane University Medical Center.

16 JOURNAL VOL 140 JULY

Jackie Tucker, LSMSA President

AUXILIARY REPORT

LUNGS FOR LIFE

REBECCA BOMBET BASILE

W HEN YOU consider that cigarette smoking is re-
sponsible for approximately 83% of all lung can-
cer and 30% of all cancer-related deaths, you might
ask yourself why? Why do people smoke?

Take a minute and reflect on several current US
statistics. One in every five high school seniors smokes
daily. Of teenagers, 10% smoke. Most teenagers begin
smoking before age 16. Most teenagers decide to smoke
by the sixth or seventh grade.

Other facts to consider include;

• There have been recent trends in smokeless tobacco
which correlate with increase in neoplasmas and
other disorders of the mouth and throat frequently
seen in young male adolescents.

• An estimated 136,000 deaths were related to limg
cancer in 1987. The age-standardized lung cancer
death rate for women is higher than that of any other
cancer. It has surpassed cancer of the breast which
was the number one cancer kiUer in women for more
than 50 years.

• Those who smoke two or more packs of cigarettes
per day have a lung cancer mortality rate 15 to 20
times greater than non-smokers.

• Smoking is related to 320,000 deaths per year with
an estimated cost from 38 to 95 billion dollars.

It is said that cigarette smoking is the largest sin-
gle preventable cause of premature death and disa-
bility in the United States. With all of this information
so readily available, again, why do people smoke?

In the fall of 1986 the St Landry Parish Medical
Auxiliary began to evaluate this information. The
American Medical Association (AMA) and AMA Aux-
iliaries had recently begun an Antismoking Public Serv-
ice Campaign promoting their policy of a smoke-free
society by the year 2000. The auxiliary decided to
promote this campaign on a local level by creating
and providing a smoking education program for the
parish youth. After joining forces with two of the local
hospM pulmonary rehabilitation programs, the re-
search began. Many available resources were evalu-
ated and the age group to be targeted was deter-
mined.

Since the decision to smoke is usually made by
the sixth or seventh grade, the educational program
was presented to fourth, fifth, and sixth graders only.
After reviewing several films, the film "'Why People ►

JOURNAL VOL 140 JULY 19

Smoke" was chosen, and was purchased with funds
provided by the St Landry Parish Medical Society.
This is a 10-minute color cartoon depicting four rea-
sons why people smoke. Once the film was acquired
and a one-hour presentation was developed, the pro-
gram was presented to the St Landry School Board
representative who authorized use of the program in
the parish schools.

The presentation consisted of an introduction
which included information on the sponsors, a brief
review of lung and heart anatomy, facts and statistics
on smoking, a teenage smoker's profile, a short dem-
onstration with plastic lungs and a cigarette, the film,
and a period for questions and answers. It was con-
cluded with a song by the American Heart Association
titled, "Smoke Is No Joke." The children were given
several handouts, including the words to the song.

The auxiliary had decided to form teams of two,
with one person to give the presentation and the other

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person to distribute the information and handle the
audio and video equipment. Eight teams were formed
which included nurses from the rehabilitation pro-
grams at both hospitals. It was the auxiliary's goal to
visit one half of the parish schools the first year and
the other half the following year. Once all the schools
had been visited, the auxiliary would only visit all
fourth graders on a yearly basis. Each team visited
two or three schools and were responsible for coor-
dinating the program with their schools.

The auxiliary named the program Lungs for Life
. . . explaining to the children that everyone gets only
one set of lungs, which makes it very important to
have all the facts before one decides to start smoking.
A logo was designed using a simple outline of the
lungs and was used on all literature given out as well
as t-shirts that were made for the auxiliary to wear
when they went to the schools. The t-shirts were so
popular with the children that the auxiliary obtained
permission from the school board to sell the shirts in
the schools with the profit going back into the pro-
gram.

The auxiliary plans to add a new aspect to the
program this year. Several high school juniors and
seniors will become part of our team. They will not
only help with the presentation but will also help sell
the t-shirts in the school. It is felt that this will serve
as positive role models for the younger children and
positive peer pressure in the high schools.

The program, in its second year, has been quite
successful. It has been positively received both by the
schools and the children and the community. The
auxiliary has been invited to participate in parades
and health fairs. The Girl Scouts have asked for the
program as well as other groups.

Today there are over 40 million nonsmokers in
the United States. Education is the key factor in this
healthy change. If we want to impact the future adults
of this country, then the best place to start is with
our children . . . which is what our auxiliary is doing.

And we are telling them . . . "Smoke is no joke."

Mrs Basile (wife of Michael W. Basile, MD) is the president of the St
Landry Parish Medical Society Auxiliary and the Community Relations
Health Coordinator at Opelousas General Hospital.

20 JOURNAL VOL 140 JULY

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THE FIVE HORSEMEN OF
RHEUMATOLOGY

JACK WAXMAN, MD

24 JOURNAL VOL 140 JULY

The aging musculoskeletal system is prone to
painful articular and para-articular syndromes
which mimic one another with similar historical
and physical clues. The physician's tendency is to
lump these overuse conditions together and
provide a nonsteroidal anti-inflammatory drug for
therapy. Herein are the clues to effectively
differentiate these five "itises" and thus manage

them more specifically.

F ive rheumatologic ills tend to occur in the aged
patient group, and often several appear in the same
individual. The five "itises" are osteoarthritis, bur-
sitis, tendinitis, neuritis, and fibrositis. Separating
them can be quite challenging; nevertheless, it is im-
portant since management of each differs. For the
most part, they are painful joint and para-articular
syndromes based on overuse, abuse, or obesity with
too many repetitions or too much load exerted upon
tendons, bursae, or joints. In fibrositis, however, ex-
cess pain in muscles occurs via sleep deprivation, anx-
iety, and depression. An underlying "itis" is also
present in the majority of fibrositis patients who are
thus considered to have "secondary" fibrositis as op-
posed to the less common primary disease.^ Osteoar-
thritis and especially fibrositis (90%) are more com-
mon in females, with menopausal aggravation
common to both ills.

OSTEOARTHRITIS

In osteoarthritis, 20 years of joint impulse loading
leads to fibrillation, cartilage loss, spur formation, and
increased capsular thickening of multiple joints, es-
pecially distal finger joints, knees, hips, neck, and
back. There is a secondary, usually modest but oc-
casionally intense, inflammatory response based on
cartilaginous debris and/or crystalline deposition. Pain
after joint use is common, especially by evening, but
morning stiffness is usually for less than 15 minutes.
Tenderness is prominent at the worn-down area of
the joint (for example, a medial joint line of the knee
or the lateral patellofemoral grove) with local crepi-
tation on movement. An x-ray film will often reveal
definite arthritis even though only 50% (or less) of
radiographically visible osteoarthritic sites are symp-
tomatic.

In management, first take care to exclude the other

"itises," which can rnirnic osteoarthritis by similar post
work pain, and then prescribe joint rest, isometric
muscle strengthening, weight loss, and an episodic
anti-inflammatory regimen keyed to the overuse pat-
terns.

TENDINITIS AND BURSITIS

Mimicry of osteoarthritis commonly occurs at the
shoulder and hip where the more common painful
syndromes are rotator cuff tendinitis with associated
subdeltoid bursitis and gluteal tendinitis with tro-
chanteric bursitis. Tenderness upon palpation local-
izes soreness at the lateral subacromial margin in the
former condition and at the trochanter in the latter.

In trochanteric bursitis, pain spreads laterally down
the limb and usually stops at the next joint; occasion-
ally, however, it goes beyond this point to the ankle.
There is restriction of external rotation in both con-
ditions, but internal rotation is more limited, partic-
ularly in hip osteoarthritis.

At the elbow, tendinitis usually occurs laterally
at the epicondyle, while bursitis occurs posteriorly at
the olecranon and may be septic (Staphylococcus au-
reus), gouty, or traumatic. At the knee, bursitis occurs
anteriorly or posteriorly (anserine and prepatellar or
gastrocnemius), the latter mimicking phlebitis be-
cause knee fluid extends posteriorly into the bursal
sac which communicates with the joint in two thirds
of patients. Eventually such extension may rupture
into the calf with the full-blown phlebitic syndrome
reproduced. Knee tendinitis, especially in runners, is
lateral and occurs at the insertion of the popliteus
above the joint line, at the iliotibial tract at its tibial
insertion, or at the patellar tendon insertion in sports
that include jumping.^ At the ankle, the Achilles ten-
don is vulnerable, while in the foot or leg the posterior
tibial tendon origin or insertion may tear with pain
on overuse, particularly in runners. Knowing the ex-
act site of these tendon origins and insertions allows
definition by carefully palpating for the often tiny
tender site. Resisted isometric contraction also allows
reproduction of the pain and separates it from os-
teoarthritis.

Treatment for these painful syndromes again em-
phasizes reduced use, ice for superficial inflammatory
sites, anti-inflammatory regimens when ice is not suf-
ficient, and/or local steroid administration adjacent to ►

JOURNAL VOL 140 JULY 25

the inflammatory focus. A re-strengthening of the in-
volved muscle groups and a re-stretching of the ten-
don as it heals is important because loss of motion
from the bound-down tendon-bursal complex is com-
mon and impedes rehabilitation. This is particularly
important at the shoulder, which loses most motion
and where a ''frozen shoulder" is likely if there is
significant delay in re-stretching maneuvers.

NEURITIS

Neuritis also mimics the preceding syndromes, par-
ticularly at the shoulder and hip where C-6 and C-7
root lesions and L-4, L-5, and S-1 root syndromes
cause nerve or muscle pain in similar distributions.
Attention to distal paresthesias or frankly numb fin-
gers and toe tips helps prove the nerve origin of the
more proximal pain state. In particular, an L4-5 disc
abutting the L5 root simulates trochanteric bursitis by
causing lateral thigh and leg pain. Careful examina-
tion of the sore L-4 and L-5 spinous processes and
gluteal musculature locates the origin of this neuro-
pathy. Another important clue is that first toe dor-
siflexion strength and straight leg raising tests are
usually abnormal, particularly in a seated position.

Therapy of nerve root syndromes is based on
protecting the nerves from further entrapment or
pressure by the use of proper posture or traction.
Often, collar or corset supports, or even maximal pro-
tection with bedrest is required. Weeks or even months
of slow healing is the rule, as is also true for tendinitis,
and the patient must avoid returning to routine ac-
tivities too soon as this reaggravates the condition.

FIBROSITIS

Fibrositis patients are separated from the above pained
individuals by a more persistent, virtually continuous
pain state that tends to be diffuse, symmetric, and
tends to be inclusive of an average of 12 "tender"
points. These excessively sore muscle bellies or ten-
don insertions cause marked patient withdrawal or
recoil on gentle palpations. These patients have trou-
ble getting and staying asleep, and are often psycho-
logically disturbed with chronic depression and anx-
iety, making management difficult. Two out of three
are menopausal before they are fibrositic, and their
menopause is usually premature and often surgical.^

Therapy focuses early on physical muscle ther-
apies, especially heat (occasionally ice before stretch)

26 JOURNAL VOL 140 JULY

with massage and mobilizing techniques, and then
later on conditioning exercises. Tricyclics are com-
monly prescribed for sleep; psychotherapy and estro-
gen may be necessary as well. If the other underlying
"itises" contribute to the painful state, they must also
be managed. Despite all these efforts, chronic pain is
still the rule, with only partial therapeutic success
during months or years of treatment.

The older patient who presents with one or more
joint complaints without swelling, with normal sedi-
mentation rate, and with the changes of osteoarthritis
on joint x-ray films presents a challenge to the ex-
amining physician. He must consider four other re-
lated syndromes and differentiate them by exami-
nation techniques and historical clues. This may be a
tedious process and is often bypassed in the rushed
world of medicine, but treatments of these states will
vary and follow-up will be crucial in healing these
disorders. Moreover, since these "five horsemen" ride
together, modification of initial therapy plans to in-
clude treatments for other "itises" may well be nec-
essary. The examining physician should, therefore,
resist the impulse to simply provide an anti-inflam-
matory drug for these painful states. Although such
a drug may be helpful, it will not do justice to the
problems these syndromes pose. ■

REFERENCES

1. Wolfe F, Cathey M: Prevalence of primary and secondary fibrositis. /
Rheumatol 1982;10:965-968.

2. Brody DM: Running injuries. Clin Symp 1980;32:15.

3. Waxman J, Zatzkis SM: Fibromyalgia and menopause. Postgrad Med
1986;80:165-171.

Dr Waxman is from the Dept of Internal Medicine, Section on
Rheumatology at Ochsner Clinic and Alton Ochsner Medical

Foundation in New Orleans.

Reprint requests should be sent to Dr Waxman,
1514 Jefferson Highway, New Orleans, LA 70121.

KAWASAKI’S SYNDROME
ACCOMPANIED BY BONE MARROW

SUPPRESSION

IRWIN COHEN, MD; MICHAEL WHISTLER, MD

This article reports for the first time a
simultaneous occurrence of bone marrow
suppression and Kawasaki's syndrome (KS).
Whereas a granulocytosis and thrombocytosis
usually accompany KS, our patient experienced a
profound neutropenia and thrombocytopenia.
Although the case fulfilled the Centers for Disease
Control clinical criteria for KS, these labortory
findings so confounded the diagnostic skills of the
attending physicians that coronary aneurysms were
not looked for until late in the illness. It is likely
that the confusion was caused by the effects of
drug allergy on laboratory derived data. The
diagnosis of KS is still a clinical one.

S INCE ITS FIRST description by Kawasaki, et aP in
1967 and again in 1974, acute mucocutaneous
lymph node syndrome, or Kawasaki's syndrome (KS)
has been increasingly recognized in this country.^- ^
The syndrome is that of an acute, febrile illness of
young children with characteristic manifestations as
defined by the Centers for Disease Control (CDC).^
Common laboratory findings include polymorpho-
nuclear leucocytosis and thrombocytosis.^ We re-
cently encountered a case of KS with bone marrow
suppression. To our knowledge, this concurrence has
never been reported.

CASE REPORT

A 9-month-old black infant boy who was well until
8/12/86 when he was taken to his pediatrician with a
one-day history of fever. His temperature was 40.1°C.
A diagnosis of acute otitis media was made; he was
sent home on a combination of amoxacillin and cla-
vulanic acid. After two doses he developed an urti-
carial rash. The following day, illness day (ID) 3, still
febrile, he was taken back to his pediatrician. The CBC
was normal; CSF culture, blood culture, and serum

JOURNAL VOL 140 JULY 31

specify Adjunctive.

latex agglutination tests were normal. Medication was
changed to a combination of erythromycin and sul-
fasoxazole. Over the next two days his fluid intake
decreased and he developed diarrhea. On ID 5, he
was admitted to a private hospital for treatment of
dehydration and fever. His sclerae were injected. His
blood picture showed a hemoglobin of 10.7 g/dL, a
hematocrit of 33.3%, a white cell count of 13,100 with
a differential of 65% polymorphonuclears, 20% bands,

9% lymphocytes, 3% monocytes, 2% eosinophils, and
1% metamyelocytes and a platelet count of 294,000.
Intravenous fluids and cefuroxime therapy at 100 mg/
kg/day were started. The following day gentamicin,

7 mg/kg/day, was added because of persistent fever,
abdominal distention, and scrotal swelling. A repeat
lumbar puncture was performed with CSF findings
of protein 20 mg/dL, glucose 72 mg/dL, 12 WBCs and
3 RBCs. CSF culture and Hemophilus influenza latex
agglutination test were negative; the platelet count
had fallen to 140,000. On ID 9, the cefuroxime was
increased to 200 mg/kg/day. On ID 11, he was still
febrile; had developed edema of his hands and feet
and a generalized maculopapular eruption. The
hemoglobin level had dropped to 7.1 g/dL; the he-
matocrit was 21.5%; the platelet count was 36,000; and
the reticulocyte count was 0.1%; the white cell count
of 20,200; and a differential cell count showed 49%
polymorphonuclears, 3% bands, 43% lymphocytes,
and 5% monocytes. Gentamicin and cefuroxime were
stopped and the patient was transferred to Tulane
Medical Center.

At Tulane, on ID 11, his temperature was 39°C.

His lips were red and there were perioral fissures. He
had a diffuse erythematous rash with target lesions
on his hands and face. His feet were edematous and
his scrotum was swollen. There was a small testicular
hydrocele. Some small, bilateral axillary nodes were
noted but no cervical adenopathy. Laboratory studies
showed a hemoglobin level of 6.7 g/dL; a hematocrit
of 21.1%; a platelet count of 20,000; a white cell count
of 12,800; a differential cell count of 11% polymor-
phonuclears, 8% bands, 75% lymphocytes, and 6%
monocytes; and an erythrocyte sedimentation rate of
55 mm/hr. Both antiplatelet and antigranulocyte an-
tibodies were present. C3 and C4 were depressed. A
urinalysis showed 40-50 WBC/HPF but a negative cul-
ture. Other negative studies included: viral cultures,
antibody and antigen for hepatitis A and B viruses,
antibody for Epstein-Barr virus and cytomegalovirus, ^

32 JOURNAL VOL 140 JULY

Each capsule contains 5 mg cblordiazepoxide HCl and 2.5 mg clidinium
bromide.

Please consult complete prescribing information, a summary of which follows:

* Indications: Based on a review of this drug by the National Academy of
Sciences— National Research Council and/or other information, FDA has
classified the indications as follows:

"Possibly” effective: as adjunctive therapy in the treatment of peptic ulcer
and in the treatment of the irritable bowel S5mdrome (irritable colon, spastic
colon, mucous colitis) and acute enterocolitis.

Final classification of the less-than-effective indications requires further
investigation.

Contraindications: Glaucoma; prostatic hypertrophy, benign bladder neck
obstruction; hypersensitivity to cblordiazepoxide HCl and/or clidinium Br.
Warnings: Caution patients about possible combined effects with alcohol and
other CNS depressants, and against hazardous occupations requiring complete
mental alertness (e.g., operating machinery, driving).

Usage in Pregnancy: Use of minor tranquilizers during first trimester
should almost always be avoided because of increased risk of congeni-
tal malformations as suggested in several studies. Consider possibility
of pregnancy when instituting therapy. Advise patients to discuss
therapy if they intend to or do become pregnant.

As with aU anticholinergics, inhibition of lactation may occur.

Withdrawal symptoms of the barbiturate type have occurred after discontinuation
of benzodiazepines (see Drug Abuse and Dependence).

Precautions: In elderly and debilitated, limit dosage to smallest effective amount
to preclude ataxia, oversedation, confusion (no more than 2 capsules/day initially;
increase gradually as needed and tolerated) . Though generally not recommended,
if combination therapy with other psychotropics seems indicated, carefully con-
sider pharmacology of agents, particularly potentiating drugs such as MAO inhib-
itors, phenothiazines. Observe usual precautions in presence of impaired renal or
hepatic function. Paradoxical reactions reported in psychiatric patients. Employ
usual precautions in treating anxiety states with evidence of impending depres-
sion; suicidal tendencies may be present and protective measures necessary.
Variable effects on blood coagulation reported very rarely in patients receiving the
drug and oral anticoagulants; causal relationship not established. Inform patients
to consult physician before increasing dose or abruptly discontinuing this drug.
Adverse Reactions: No side effects or manifestations not seen with either com-
pound alone reported with Librax. When cblordiazepoxide HCl is used alone,
drowsiness, ataxia, confusion may occur, especially in elderly and debilitated;
avoidable in most cases by proper dosage adjustment, but also occasionally
observed at lower dosage ranges. Syncope reported in a few instances. Also
encountered: isolated instances of skin eruptions, edema, minor menstrual irreg-
ularities, nausea and constipation, extrapyramidal symptoms, increased and
decreased libido— aU infrequent, generally controUed with dosage reduction;
changes in EEG patterns may appear during and after treatment; blood dyscrasias
(including agranulocytosis), jaundice, hepatic dysfunction reported occasionally
with cblordiazepoxide HCl, making periodic blood counts and liver function tests
advisable during protracted therapy. Adverse effects reported with Librax typical
of antichoUnergic agents, i.e., dryness of mouth, blurring of vision, urinary hesi-
tancy, constipation. Constipation has occurred most often when Librax therapy is
combined with other spasmolytics and/or low residue diets.

Drug Abuse and Dependence: Withdrawal symptoms similar to those noted with
barbiturates and alcohol have occurred foUowing abrupt discontinuance of chlor-
diazepoxide; more severe seen after excessive doses over extended periods; milder
after taking continuously at therapeutic levels for several months. After extended
therapy, avoid abrupt discontinuation and taper dosage. Carefully supervise
addiction-prone individuals because of predisposition to habituation and
dependence.

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When it's brain versus bowel,

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In irritable bowel syndrome,* intestinal
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anxiety— launching a cycle of brain/bowel
conflict. Make peace with Librax. Because of
possible CNS effects, caution patients about
activities requiring complete mental alertness.

*Librax has been evaluated as possibly effective
as adjunctive therapy in the treatment of peptic
ulcer and IBS.

Specify Adjunctive

Each capsule contains 5 mg chlordiazepoxide
HCl and 2.5 mg cUdinium bromide.

Please see summary of prescribing information on adjacent page.

antinuclear antibody, Coombs' test, stool culture, and
stool hematest. A bone marrow aspiration and biopsy
performed on ID 12 showed an increased number of
megakaryocytes with suppression of both the eryth-
rocyte and granulocyte precursors, and plasmacyto-
sis.

Fever persisted until ID 23. The rash resolved on
ID 22 at which time periungual and generalized des-
quamation were noted. Serial CBCs showed a persis-
tant microcytic anemia, thrombocytopenia, neutro-
penia (the absolute neutrophil count was less than
1,000 from ID 17 to ID 23), and lymphocytosis. The
reticulocyte count began to increase on ID 19. Throm-
bocytopenia resolved on ID 23. The maximum platelet
count was 533,000 on ID 26.

A 2D echocardiogram on ID 23 showed large,
diffuse, sausage-shaped coronary artery aneurysms
with a moderate pericardial effusion. Aspirin therapy
was started at 10 mg/kg/day. On ID 29 the ECG showed
Q waves present in the inferior leads. Serial cardiac
isoenzymes were negative. A repeat echocardiogram
showed some dyskinesis of the inferior portion of the
intraventricular septum. A multigated acquisition scan
showed a normal ejection fraction. A thallium scan
showed decreased tracer uptake in the inferior region
of the heart. After the resolution of the pericardial
effusion, the infant was discharged to the care of his
pediatrician. As of this writing, he is doing well.

COMMENT

The CDC defines KS as an illness characterized
by unexplained fever for longer than 5 days and at
least four of the following: 1) bilateral conjunctival
injection; 2) mucous membrane changes, including
injected, dry or fissured lips, pharyngeal injection and
strawberry tongue; 3) changes in the extremities, in-
cluding erythema of the palms and soles, edema of
the hands or feet, and generalized or periungual des-
quamation; 4) rash; 5) cervical adenopathy. Other
commonly reported findings include sterile pyuria,^' ^
diarrhea,^' ^ and elevated liver enzymes.^' ^ Approxi-
mately 20% of all cases develop aneurysms of the
coronary arteries.^- ^ At the time that the coronary ar-
tery aneurysms are discovered, a thrombocytosis and
a polymorphonuclear leukocytosis are seen. This is
usually during the second or third week of the illness.^

During that period in our patient's illness, throm-
bocytopenia and neutropenia were observed. A bone

34 JOURNAL VOL 140 JULY

marrow aspiration showed suppression of erythro-
cyte and granulocyte precursors. These changes have
not been reported with KS. They are seen with viral
infection®' ^ and drug allergy. These associations made
viral infection or drug allergy the most probable causes
of this patient's prolonged illness.

This case did, however, fulfill the CDC clinical
criteria for KS even before the echocardiogram was
obtained. It is possible that more than one pathologic
process occurred. The clinical course and the almost
pathognomonic findings of coronary aneurysms and
infarct make a diagnosis of KS unavoidable. The neu-
tropenia and thrombocytopenia suggest a second
process which, in this case, is more likely due to drug
allergy than a simultaneous viral infection. The pres-
ence of antibodies to platelets and granulocytes, of
depressed complement levels, of negative viral cul-
tures, and of negative serologic studies support this
conclusion.

The rapid, presumptive diagnosis of KS consist-
ent with CDC clinical guidelines is important. Treat-
ment of patients with KS with aspirin and intravenous
immunoglobulin within 10 days of the onset of fever
has proven to be effective in reducing the formation
of coronary artery aneurysms. This patient was not
found to have aneurysms until ID 23 because the proc-
ess of making a clinical diagnosis of KS was con-
founded by the drug allergy induced hematologic
findings. By then the therapeutic window was closed.
It should be emphasized, especially because timely
therapy is effective in improving outcome, that KS is
a clinical diagnosis and that, at present, laboratory
findings can play only a supportive role. ■

REFERENCES

1. Kawasaki T, Kosaki F, Okgwa S, et al: A new infantile acute febrile
mucocutaneous lymph node syndrome prevailing in Japan. Pediatrician
1974;54:271-276.

2. Bell DM, Morens DM, Holman R, et al: Kawasaki syndrome in the United
States. Am J Dis Child 1983;137:211-214.

3. MeUsh ME: Kawasaki syndrome: A new infectious disease? J Infect Dis
1981;143:317-324.

4. Morens DM, Anderson L, Hurwitz E, et al: National surveillance of
Kawasaki disease. Pediatrics 1980;65:21-25.

5. Dean AG, Melish M, Hicks R, et al: An epidemic of Kawasaki syndrome
in Hawaii. J Pediatr 1982;100:552-557.

6. Black CA, Bocchini J, Everist J, et al: Mucocutaneous lymph node syn-
drome in north Louisiana: Review of 15 cases. South Med J 1983;76:290-
295.

7. Nakano H, Saito A, Ueda K, et al: Clinical characteristics of myocardial
infarction following Kawasaki disease: Report of 11 cases. / Pediatr
1986;108:198-203.

8. Blacklock HA, Mortimer PP: Aplastic crisis and other effects of human
parvovirus infection. Clin Haeeamatol 1984;13:679-691.

9. Yoimg N, Mortimer P: Viruses and bone marrow failure. Blood 1984;63:729-
737.

10. VanArsdel PP Jr: Drug allergy: An update. Med Clin North Am 1981;65:1089-
1102.

11. Newburger JW, Takahashi M, Bums JC, et al: The treatment of Kawasaki
syndrome with intravenous gamma globulin. N Engl J Med 1986;315:341-
347.

Drs Cohen and Whistler are from the Dept of Pediatrics at Tulane
University School of Medicine in New Orleans.

Reprints will not be available.

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JOURNAL VOL 140 JULY

CESAREAN CHILDBIRTH RATE
AMONG WOMEN IN THE
NEW ORLEANS AREA

JOAN H. WIGHTKIN, MPH; LINDA M. LAMBERT, MPH

The national rate of cesarean section delivery more
than doubled between 1975 and 1985, from 10.4 to
22.7. In 1984, when the US cesarean delivery rate
was 21.1 cesareans per 100 deliveries, a Southeast
Louisiana Health Cost Management, Inc study
entitled Medical Cost Utilization Study, 1984
showed a cesarean childbirth rate of 34.8 per 100
deliveries for 656 deliveries in the New Orleans
metropolitan area. This article presents the results
of an indepth survey of the cesarean section rates
for hospitals, insurance carriers, Medicaid, and
Charity Hospital for the New Orleans area. The
1985 cesarean rate for 15 New Orleans area
hospitals including Charity Hospital was 28.2 per
100 deliveries, which was higher than the national
(22.7) and southern (23.5) rate. The cesarean
section rate for insured women in New Orleans
was significantly higher than that for the Medicaid
and Charity Hospital population. The rate of
increase in cesarean sections in the New Orleans
area is also examined. This article outlines the
factors contributing to the increasing cesarean
delivery rate nationwide and calls for action on the
part of the medical community.

Physicians from the Orleans, Jefferson, and St Bernard
parish medical societies provided significant input into the
preparation of this study. Physicians who were members of
Southeast Louisiana Health Cost Management's Medicine!
Industry Task Force, as well as guest physicians, analyzed
all of the extensive data and informational materials collected
in order to report the facts as simply as possible. The fol-
lowing report was reviewed by these physicians for its med-
ical appropriateness and its accuracy. It points out the need
for further study to determine the reasons for the higher
than average rate of cesarean sections in New Orleans.

T he dramatic increase in the number of cesarean
deliveries performed nationwide over the past 15
years warrants close examination by providers, con-
sumers, and payors of health care.

In 1975, 10.4 per 100 deliveries in the United States
were by cesarean childbirth. By 1985, that figure had
more than doubled to 22.7 (Table 1).^' ^ That year, the
southern region had the highest rate (23.5) of the four
regions of the United States.

In 1984, when the national rate was 21.1 cesar-
eans per 100 deliveries, a Southeast Louisiana Health ►

journal VOL 140 JULY 39

TABLE 1

US CESAREAN DELIVERY RATES PER 100 DELIVERIES

Cesarean

Year

Rate

1970

5.5

1975

10.4

1980

16.5

1985

22.7

Source of data: Taffel SM, Placek PJ, Liss TL: Trends in the
United States cesarean section rate and reasons for the 1 980-
1 985 rise. Am J Public Health 1 987.

Cost Management Inc (SLHCM) study entitled Med-
ical Cost Utilization Study, 1984, showed a cesarean
childbirth rate in 656 deliveries at 34,8 for the New
Orleans metropolitan area. The data for this study
were medical claims from 13 employer groups and a
group of 2,500 small companies who insured 75,628
people. The high cost and the frequency of this sur-
gical procedure motivated the authors to look further
at the cesarean childbirth rate by gathering more sub-
stantial data and presenting them in this report to the
medical community.

METHOD

A survey was mailed to 21 New Orleans area hos-
pitals, the Metropolitan Hospital Council of New Or-
leans, and 18 insurers, third party administrators.
Health Maintenance Organizations (HMO), and Pre-
ferred Provider Organizations (PPO). The informa-
tion requested on the survey was: the total number
of deliveries, the number of cesarean deliveries, the
number of primary cesarean deliveries, and the num-
ber of repeat cesarean deliveries for each year from
1981 through 1986 in the New Orleans area. The sur-
vey indicated that company/hospital names would be
kept confidential if requested.

The Metropolitan Hospital Council of New Or-
leans provided aggregate data for 14 area hospitals
covering all 1985 admissions together with a break-
down of births by age of the mother, payor source,
and method of delivery. Also, six hospitals responded
individually to the survey. Data from one hospital
were not used because the data covered years 1981

40 JOURNAL VOL 140 JULY

through 1983 only. Four hospitals provided primary
and repeat cesarean section statistics. One HMO and
one PPO answered the survey. Five insurers re-
sponded to the survey. In addition, data were ex-
tracted from a proprietary insurance data base which
includes a number of insurance company statistics.
This data base is reported as Aggregate Insurance
Data and may include some of the other five insurers
responding to the survey. The presentation of data is
limited to the Metropolitan Hospital Council, Charity
Hospital, four individual hospitals, and the Aggregate
Insurance Data.

RESULTS

The Metropolitan Hospital Council of New Orleans'
data base showed a cesarean section rate of 32.8 per
100 deliveries for 10,276 deliveries with 3,367 cesarean
sections for 1985. The 1985 rate for Charity Hospital
of New Orleans was 20.4 per 100 deliveries for 5,927
deliveries with 1,208 cesareans performed. For the 14
hospitals included in the Metropolitan Hospital
Council data base plus the Charity Hospital of New
Orleans data, the cesarean section rate was 28.2 per
100 deliveries. The true cesarean section rate lies be-
tween 27.5 per 100 and 28.9 per 100 with a confidence
of 97.5, which is approximately two standard devia-
tions. This was based on 16,203 deliveries with 4,575
cesarean sections and represents 71.8% of all births
occurring in Orleans and Jefferson parishes. In 1985,
the New Orleans area cesarean section rate was higher
than the national rate and higher than the rate for the
southern region. From Table 2, the difference can also
be observed when the Metropolitan Hospital Council
data are broken down by the age of the mother.

The New Orleans area hospital cesarean delivery
rates as reported by individual hospitals are higher
than the national average except for Charity Hospital
of New Orleans (Fig 1). The average annual increase
in the national cesarean section rate between 1981 and
1986 was 1.2 percentage points per year. The average
increase per year for each of the New Orleans hos-
pitals reporting data for 1981 to 1986 was: Hospital 1,
2.0 percentage points per year; Hospital 2, 1.3 per-
centage points per year; Hospital 3, 2.3 percentage
points per year. The cesarean section rate for Hospital
4 increased 4.0 percentage points from 1985 to 1986.
The cesarean section rate for Charity Hospital of New
Orleans decreased 0.5 percentage points from 1985 to
1986.

TABLE 2

CESAREAN SECTION RATES (PER 100 DELIVERIES) FOR NON-FEDERAL SHORTSTAY HOSPITALS
FOR THE UNITED STATES, THE SOUTH, AND THE NEW ORLEANS AREA

Metropolitan

Hospital

Charity

Council of

Hospital

United

New Orleans

of New

States

South

Data*

Orleans

C-Section
Rate for
the New
Orleans
Areaf

Total

Age of Mother
(Years)

22.7

23.5

32.8

(10,276)

deliveries

<20

16.1

16.0

27.0

20-24

21.2

22.6

29.1

25-29

22.9

23.4

33.2

30-34

26.6

30.7

37.5

35>

30.7

30.6

43.8

20.4

(5,927)

deliveries

28.2

(16,203)

deliveries

Source of data: For the United States and the South: Placek PJ, Taffel S, Moien M; Cesarean rate increase in 1985. Am J Public Health
1987;77:241-242. New Orleans rates: Metropolitan Hospital Council of New Orleans and Charity Hospital of New Orleans, 1985.

‘Metropolitan Hospital Council of New Orleans Data includes 1 4 area hospitals excluding Charity Hospital of New Orleans.

tCesarean rate for New Orleans area is the combined Metropolitan Hospital Council of New Orleans data and Charity Hospital of New
Orleans data.

hospital #4

hospital #3

■ hospital #2

hospital #1

■Hi USA

Charity

Hospital at
New Orleans

Source of data: For United States: Placek
PJ, Taffel SM, LissTL: The cesarean future.
American Demographics 1987. For New
Orleans: Self-reported by five New Orleans
hospitals.

Fig 1. Cesarean delivery rate per 100 deliveries for the United States and five New Orleans area hospitals.

JOURNAL VOL 140 JULY 41

TABLE 3

CESAREAN DELIVERY RATES FOR A SEGMENT OF THE INSURED POPULATION OF NEW ORLEANS

AGGREGATE INSURANCE COMPANY DATA

Total

Year

Rate

Deliveries

Cesarean

1983

27.6

3128

863

1984

29.4

6363

1873

1985

33.6

8296

2790

1986

38.8

8267

3210

rate

per

100

deliveries

83 84 85 86

years

Source of data: Aggregate Insurance Company Data for the New Orleans area, 1 987.

TABLE 4

CESAREAN SECTION RATE BY EXPECTED SOURCE OF PAYMENT FOR THE UNITED STATES AND THE
SOUTHERN REGION COMPARED WITH THE CESAREAN SECTION RATE FOR 8,495 DELIVERIES IN
FOURTEEN NEW ORLEANS HOSPITALS EXCLUSIVE OF CHARITY HOSPITAL OF NEW ORLEANS

Medicaid Blue Cross Other Commercial Insurance

United

States

South

New

Orleans

United

States

South

New

Orleans

United

States

South

New

Orleans

Total

20.1

19.4

25.60-29.00*

24.6

24.2

32.40-38.93*

24.7

27.1

35.39-38.21*

Age of Mother
(years)
<30

18.9

N/A

27.1

23.2

N/A

32.8

23.0

N/A

33.7

>30

29.2

N/A

29.0

27.5

N/A

40.0

28.5

N/A

42.5

Source of data: National and southern rates: Tabulation from the National Center for Health Statistics from National Hospital Discharge
Survey, 1985. New Orleans rates: Metropolitan Hospital Council of New Orleans Data, 1985.

‘The true rate is expected to tie in this interval with a 97.5% confidence.

Primary cesarean section rate is defined as the
ratio of the number of first cesarean sections to the
number of mothers who never had a cesarean section.
The primary cesarean section rate is predictive of the
rate of increase in the overall cesarean section rate
because subsequent births will likely be sections.^ In
1985, the primary cesarean section rate for the four

New Orleans hospitals with 4,132 deliveries was 24,3
compared to the primary cesarean section rate for the
United States of 16.3. The true primary rate for New
Orleans hospitals would be between 22.86 and 25.74
with a 97.5% confidence, which is approximately two
standard deviations. The primary rate for the United
States increased 1.1 percentage points between 1985

42 JOURNAL VOL 140 JULY

and 1986 to 17.4 while the primary rate for the four
New Orleans hospitals increased 2.8 percentage points
from 24.3 to 27.1. The true primary rate for the four
New Orleans hospitals for 1986 was between 25.74
and 28.53 with a confidence of 97.5%, which is ap-
proximately two standard deviations.

Aggregate Insurance Data provided a large sample
of insured deliveries in the New Orleans area. In 1986,
there were 8,267 deliveries with 3,210 cesarean deliv-
eries yielding a cesarean delivery rate of 38.8 per 100
deliveries (Table 3). The national cesarean section rate
increased 3.8 percentage points from 20.3 in 1983 to
24.1 in 1986. In the Aggregate Insurance Data, the
cesarean section rate increased 11.2 percentage points
between 1983 and 1986, from 27.6 to 38.8.

The Metropolitan Hospital Council of New Or-
leans data base was broken down by expected source
of payment for comparison with national data. The
cesarean section rate for New Orleans was statistically
significantly higher than the rate for the United States
and the South in three payor categories: Medicaid,
Blue Cross, and Other Commercial Insurance (Table
4). Among Medicaid patients, the rate of cesarean
deliveries was statistically significantly lower than the
rate for patients covered by Blue Cross and Other
Commercial Insurance in New Orleans. Similar trends
can be observed when the data is broken down by
the age of the mother, with the greatest difference
occurring between the United States rates and the
rates in New Orleans for Blue Cross and for Other
Commercial Insurance Companies (Table 4).

Most
patients
need
only one.

DISCUSSION

This study demonstrates that the cesarean section rate
in New Orleans exceeds both the national and south-
ern regional rates. The cesarean section rate for the
insured patient is significantly higher than that for
Medicaid and Charity Hospital patients. Among the
four hospitals submitting data on primary cesarean
sections, the primary section rate significantly ex-
ceeded the national rate.

The medical literature points to the following fac-
tors as the leading contributors to the increasing ce-
sarean childbirth rate.

• There has been an increase in the diagnosis of dys-
tocia and fetal distress and the subsequent use of
cesarean section as intervention.^

• The use of cesarean delivery for breech presentation

has increased from 14.8% in 1970 to 80.7% in 1985. ^ ►

Microburst

Release

System"

(potassium chloride) 20mEq

A daily prophylactic dose
in a single tablet.

Please see next page for brief summary of prescribing information.

Pharmaceuticals, Inc.
Kenilworth, NJ 07033

World leader in drug delivery systems.

K->UH

(potassium chloride)

Microburst

Fielease

System"

Sustaned Release Tablets

INDICATIONS AND USAGE; BECAUSE OF REPORTS OF INTESTINAL AND GASTRIC ULCERATION AND
BLEEDING WITH SLOW-RELEASE POTASSIUM CHLORIDE PREPARATIONS, THESE DRUGS SHOULD
BE RESERVED FOR THOSE PATIENTS WHO CANNOT TOLERATE OR REFUSE TO TAKE LIQUID OR EF-
FERVESCENT POTASSIUM PREPARATIONS OR FOR PATIENTS IN WHOM THERE IS A PROBLEM OF
COMPLIANCE WITH THESE PREPARATIONS.

1. For therapeutic use in patients with hypokalemia with or without metabolic alkalosis, in digitalis
intoxication and in patients with hypokalemic familial periodic paralysis.

Wax-matrix potassium chloride preparations have produced esophageal ulceration in certain cardi-
ac patients with esophageal compression due to enlarged left atrium.

WARNINGS; Hyperkalemia— In patients with impaired mechanisms for excreting potassium, the ad-
ministration of potassium salts can produce hyperkalemia and cardiac arrest. This occurs most com-
monly in patients given potassium by the intravenous route but may also occur in patients given
potassium orally. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of
potassium salts in patients with chronic renal disease, or any other condition which impairs potas-
sium excretion, requires particularly careful monitoring of the serum potassium concentration and
appropriate dosage adjustment.

K-DUR tabiets contain micro-crystalioids which disperse upon disintegration of the tablet. These
micro-crystalloids are formulated to provide a controlled release of potassium chloride. The dispersi-
bility of the micro-crystalloids and the controiled release of ions from them are intended to minimize
the possibility of a high local concentration near the gastrointestinal mucosa and the ability of the KOI
to cause stenosis or ulceration. Other means of accomplishing this (e.g., incorporation of potassium
chloride into a wax matrix) have reduced the frequency of such lesions to less than one per 100,000
patient years (compared to 40-50 per 100,000 patient years with enteric-coated potassium chloride)
but have not eliminated them. The frequency of Gl lesions with K-DUR tablets is, at present,
unknown. K-DUR tabiets shouid be discontinued immediately and the possibility of bowel obstruction
or perforation considered if severe vomiting, abdominal pain, distention, or gastrointestinal bleeding
occurs.

PRECAUTIONS: The diagnosis of potassium depletion is ordinarily made by demonstrating hypokale-
mia in a patient with a clinical history suggesting some cause for potassium depletion. In interpreting
the serum potassium level, the physician should bear in mind that acute alkalosis per se can produce
hypokalemia in the absence of a deficit in total body potassium while acute acidosis per se can in-
crease the serum potassium concentration into the normal range even in the presence of a reduced
total body potassium. The treatment of potassium depletion, particularly in the presence of cardiac
disease, renal disease, or acidosis requires careful attention to acid-base balance and appropriate
monitoring of serum electrolytes, the electrocardiogram, and the clinical status of the patient.

Drug Interactions: Potassium-sparing diuretics; see WARNINGS.

Carcinogenesis, Mutagenesis, impairment of Fertility: Long-term carcinogenicity studies in
animals have not been performed.

Pregnancy Category C: Animal reproduction studies have not been conducted with K-DUR. It is
also not known whether K-DUR can cause fetal harm when administered to a pregnant woman or can
affect reproduction capacity. K-DUR should be given to a pregnant woman only if clearly needed.

Nursing Mothers; The normal potassium ion content of human milk is about 13 mEq per liter. Since
oral potassium becomes part of the body potassium pool, so long as body potassium is not exces-
sive, the contribution of potassium chloride supplementation should have little or no effect on the
level in human milk.

Pediatric Use: Safety and effectiveness in children have not been established.

ADVERSE REACTIONS: One of the most severe adverse effects is hyperkalemia (see CONTRAINDICATIONS,
WARNINGS, and OVERDOSAGE). There have also been reports of upper and lower gastrointestinal
conditions including obstruction, bleeding, ulceration, and perforation (see CONTRAINDICATIONS
and WARNINGS); other factors known to be associated with such conditions were present in many of
these patients.

Skin rash has been reported rarely.

OVERDOSAGE: The administration of oral potassium salts to persons with normal excretory mecha-
nisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are im-
paired or if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can
result (see CONTRAINDICATIONS and WARNINGS). It is important to recognize that hyperkalemia is
usually asymptomatic and may be manifested only by an increased serum potassium concentration
and characteristic electrocardiographic changes (peaking of T-waves, loss of P-waves, depression of
S-T segment, and prolongation of the QT-interval). Late manifestations include muscle-paralysis and
cardiovascular collapse from cardiac arrest.

Treatment measures for hyperkalemia include the following:

1. Elimination of foods and medications containing potassium and of potassium-sparing diuretics.

2. Intravenous administration of 300 to 500 ml/hr of 10% dextrose solution containing 10-20 units
of insulin per 1,000 mi,

3. Correction of acidosis, if present, with intravenous sodium bicarbonate.

4. Use of exchange resins, hemodialysis, or peritoneal dialysis.

In treating hyperkalemia, it should be recalled that in patients who have been stabiiized on
digitaiis, too rapid a lowering of the serum potassium concentration can produce digitalis toxicity.

1002004

Key Pharmaceuticals, Inc.

Kenilworth, NJ 07033 (USA)

World leader in drug delivery systems.

13944326
Rev. 4/87

• There is continual adherence to the standard “once
a cesarean, always a cesarean," a phrase originated
in 1916 by Dr E. B. Craigin. Of women with pre-
vious cesarean deliveries giving birth in 1985, 93%
had repeat cesarean deliveries.^

• The fear of litigation and practice of defensive med-
icine is a problem in obstetrics. Before 1976, mal-
practice suits were filed each year against 1 in 20
obstetricians; by 1985 that proportion had increased
to 1 in 6.^

The New Orleans area data are consistent with find-
ings in the medical literature which show that the
insured status of a patient has an effect on cesarean
delivery rates. ^ In 1985, the New Orleans Medicaid
population had a cesarean section rate of 27.3 per 100
deliveries (2,726 Medicaid deliveries) and the Blue
Cross and other commercially insured New Orleans
area population had a rate of 36.5 per 100 deliveries
(5,769 insured deliveries). The difference between the
cesarean section rate for Medicaid and insured pa-
tients was 4 percentage points in the national data
and 9 percentage points in the New Orleans data.

The medical necessity of the New Orleans area
cesarean delivery rate warrants further investigation.
In light of the complex medical, legal, and insurance
issues, a multidisciplinary committee could be estab-
lished to develop policy recommendations for local
hospitals, providers, and consumers with respect to
the local cesarean section rate. By taking a closer look
at the issues surrounding the high cesarean rate in
New Orleans, the medical community can maintain
its position of leadership and its protection of the
standard of quality of care. ■

REFERENCES

1. Taffel S, Placek PJ, Liss TL; Trends in the United States cesarean section
rate and reasons for the 1980-85 rise. Am J Public Health 1987;77:955-959.

2. Placek PJ, Taffel S, Moien M: Cesarean rate increase in 1985. Am J Public
Health 1987;77:241-242.

3. Shiono PH, Fielden JC, McNellis D, et al: Recent trends in cesarean birth
and trial of labor rates in the United States. JAMA 1987;257:494-497.

4. Casselberry E: Forum on malpractice issues in childbirth. Public Health
Rep 1985;100:629-633.

5. Placek PJ, Taffel S. Complications in cesarean and non-cesarean deliveries:
United States, 1980. Am J Public Health 1983;73:856-862.

Ms Wightkin is the coordinator of the Special Supplemental Food
Program for Women Infant and Children (WIC) for the Louisiana Dept

of Health £r Hospitals. Formerly the director of the Louisiana Maternal
and Child Health Program, she directed the nationally recognized
improved Pregnancy Outcome Project. Ms Wightkin is a graduate of
Boston University and Tulane University School of

Public Health.

Ms Lambert is executive director of Southeast Louisiana Health Cost
Management, Inc. Recognized for leadership by the National Council on
Family Relations, Ms Lambert is a graduate of Louisiana State
University and the University of North Carolina School of

Public Health.

Reprint requests should be sent to Linda M. Lambert, Executive
Director, Southeast Louisiana Health Cost Management, Inc,
1440 Canal St, Suite 1704, New Orleans, LA 70112.

Acknowledgments to the following individuals, who contributed
professional expertise to this project. Medical society members: Lynn
Hickman, MD; Jay Shames, MD; George Ellis, MD; K. Barton Farris,
MD; Vincent Culotta, MD; W’illiam Renaudin, MD; Warren Plauche,
MD; Frank George, MD; Alarise Gottlieb, MD. National Center for
Health Statistics: Paul Placek, PhD; Selma Taffel; Gregory Pappas,
MD, PhD. Industry representatives: Christfried Unier. MD; Warren
Perkins; Erling Hamjnarstrom; G. Edward Woodmansee; Carolyn
Aides. Aietropolitan Hospital Council of New Orleans: John Finn, PhD;
Karin Brown. Charity Hospital at New Orleans: Elliott Roberts;

Joseph Aiiller, MD.

JOURNAL VOL 140 JULY 45

Re-introduce The Oldest
Advance In Medicines.

It’s called talking. Right or wrong, many older people today
feel that doctors just don’t spend as much time talking
with their patients as they used to. Things seem more
rushed and hurried.

But talking, especially about medicines, is more important
than ever before. Your older patients may be taking several
different medicines and seeing more than one doctor. And
many older people are treating themselves with over-the-
counter drugs.

Unfortunately, an older person’s response to medicines is
less predictable than a younger person’s. They can experience
altered drug actions and adverse drug reactions.

So, if they don’t tell you first, ask them what they’re taking
and if the medicines are causing any problems. Take a
complete medications history including both prescription
and non-prescription medicines.

Make it a point to tell them what they need to know — the
medicine’s name, how and when to take it, precautions, and
possible side effects. Give them written or printed information
they can take home, and encourage them to write down
what you tell them.

Good, clear communication about medicines can increase
compliance, prevent problems, and lead to better health.

So re-introduce the oldest advance in medicines. Make
talking a crucial part of your practice. It isn’t a thing of the
past. It’s the way to a healthier future.

Before they take it,
talk about it.

^ National Council on

Patient Information and Education.
666 Eleventh St. N.W. Suite 810
Washington, D.C. 20001

PHYSICIAN
SPECIALISTS.

The Air Force can make you an attractive
offer — outstanding compensation, better
working hours plus opportunities for
professional development. You con hove
o challenging practice and time to
spend with your family. Find out what the
Air Force offers a specialist up to age 58.
Call

Capt Frederick
(817) 640-6469

COLLECT

Physicians Recognition Award

Nineteen physicians from the state of Louisiana were awarded the Physicians Recognition Award [PRA] during
April, 1988. This award is presented by the American Medical Association to physicians who have voluntarily
completed 1 50 hours of continuing medical education during a consecutive three-year time period. Of these 1 50
hours, at least 60 must be in AMA/PRA Category 1 . These nineteen individuals and the cities in which they reside
are presented below.

Bastrop

James Michael Smith, MD

Jefferson

Sandra Kathleen Mahkorn, MD

Baton Rouge

Henry Raoul Olivier, MD

Coushatta

Fred Spencer Willis, MD

DeRidder

John Errol McMillan, MD

Gretna

Charles Hunter Watts, MD

Lafayette

Stephen Ira Goldware, MD

Lake Charles

Clark Alan Gunderson, MD

Metairie

Peter Charles Horowitz, MD

Houma

Harold Theodore Conrad, MD

Monroe

Alfred Dent Tisdale, MD

New Orleans

H. Russell Albright, MD
Robert T. Cook III, MD

Opelousas

Henry E. McLemore II, MD
Michael H. Montgomery, MD

Ringgold

Don Gregory Bell, MD

Shreveport

Richard Denman Crow, MD
Edward H. Leatherman, MD
Baer Irwin Rambach, MD

All recipients are members of the Louisiana State Medical Society.

CALENDAR

August

August 13-14

Anesthesia for the Cardiac Patient Having Non-Cardiac
Surgery, San Diego. Contact: American Society of Anesthe-
siologists, 515 Basse Hwy, Park Ridge, IL 60068.

Discussions of Current Hand Care Concepts, San Diego.
Contact: Plastic Surgery Educational Foundation, 444 East Algon-
quin Rd, Arlington Heights, IL 60005; (312)228-9900.

August 14-19

Wilderness Medicine, Snowmass, Colorado. Contact: Office
of Continuing Medical Education, UC San Diego School of
Medicine, M-017, La Jolla, CA 92093-0617; (619)534-3940.

August 18-21

Discussions of Current Hand Care Concepts, San Diego.
Contact: Plastic Surgery Educational Foundation, 444 East Algon-
quin Rd, Arlington Heights, IL 60005; (312)228-9900.

August 21-30

INTRAV Cruise on the Queen Elizabeth 2 and London, Con-
tact: Anita Bums, Louisiana State Medical Society, 1700 Josephine
St, New Orleans, LA 70113; (504)561-1033, (800)462-9508.

August 27

Teleplast Teleconference on Fasciocutaneous Flaps,

Metairie, Shreveport, and Baton Rouge, Louisiana. Contact:
Plastic Surgery Educational Foundation, 444 East Algonquin Rd,
Arlington Heights, IL 60005; (312)228-9900.

September

September 6-9

3rd Annual Plastic Surgery of the Breast Symposium, San-
ta Fe, New Mexico. Contact: Plastic Surgery Educational Foun-
dation, 444 East Algonquin Rd, Arlington Heights, IL 60005;
(312)228-9900.

September 8-9

Howto Select and Evaluate Residents, Boston. Contact: The
American Board of Medical Specialties, PO Box 1280, Evanston,
IL 60204; (312)491-9091.

September 10-18

4th Annual Fall Ultrasound Symposia, London and Paris.
Contact: Annual Fall Ultrasound Meeting, Medical Seminars In-

ternational Inc, 21915 Roscoe Blvd, Suite 222, Canoga Park, CA
91304; (818)719-7380.

September 13-16

39th Annual Conference of the American Group Practice
Association: Charting the Course, San Diego. Contact:
AGP A, 1422 Duke St, Alexandria, VA 22314; (703)838-0033.

September 14-19

Cosmetic Surgery of the Face and Breast, Monte Carlo,
Monaco. Contact: Francine Leinhardt, Conference Coordinator,
210 East 64th St, New York, NY 10021; (212)838-9200 ext 2776.

September 17-18

Metropolitan Regional Refresher Course, Las Vegas. Con-
tact: American Society of Anesthesiologists, 515 Basse Hwy, Park
Ridge, IL 60068.

September 17-19

4th Annual Meeting of the American Society for Reconstruc-
tive Microsurgery, Baltimore. Contact: ASRM, 3025 South
Parker Rd, Suite 65, Aurora, CA 80014.

September 29-30

Issues and Concerns Facing IRBs and Clincial Investigators,

Austin, Texas. Contact: Office of Continuing Medical Education,
Scott & White, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

October

October 3-5 |

NIH Consensus Development Conference: Urinary Incon- |
tinence in Adults, Bethesda, Maryland. Contact: Conference
Registrar, Prospect Associates, Suite 500, 1801 Rockville Pike,
Rockville, MD 20852; (30D468-MEET. jj

October 3-7 j

6th Annual Comprehensive Review of Vascular Siugery,

Santa Monica, California. Contact: UCLA Extension, PO Box .
24901, Los Angeles, CA 90024-0901; (213)825-1901. j

October 8-12 '

American Society of Anesthesiologists Aimual Meeting, San

Francisco. Contact: ASA, 515 Basse Hwy, Park Ridge, IL 60068.

October 8-15

10th International Seminar on Operative Arthroscopy,

48 JOURNAL VOL 140 JULY

Kauai, Hawaii. Contact: UCLA Extension, Dept of Continuing
Education, PO Box 24901, Los Angeles, CA 90024-0901;
(213)825-1901.

October 8-16

13th Annual International Body Imaging Conference, Maui,
Hawaii. Contact: Annual Body Imaging Conference, 21915 Roscoe
Blvd, Suite 222, Canoga Park, CA 91304; (818)700-9821.

October 12-14

Hip and Knee Reconstructive Surgery 1988, Kauai, Hawaii.
Contact: UCLA Extension, Health Sciences Dept, PO Box 24901,
Los Angeles, CA 90024-0901; (213)825-1901.

October 22-23

Review Course in Pediatric Orthopaedics, New Orleans.
Contact: Children's Hospital, Dept of Orthopaedics, 200 Henry
Clay Ave, New Orleans, LA 70118; (504)891-7067.

October 26-30

AMA 9th National Conference on Impaired Health Profes-
sionals: Visions and Values, Chicago. Contact: AMA, 535
North Dearborn St, Chicago, IL 60610; (800)621-8335.

November

November 2-5

Optimizing Management of Primary Bone Tumors: An In-
ternational Symposium Emphasizing the Multidisciplinary
Approach, Houston. Office of Conference Services, M.D. Ander-
son Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030;
(713)792-2222.

November 5

November 10-13

Lasers for the Plastic Surgeon, Orlando, Florida. Contact:
Plastic Surgery Educational Foundation, 444 East Algonquin Rd,
Arlington, Heights, IL 60005; (312)228-9900.

November 11-12

November 17-20

Assuring the Future Fiscal Survival of Consultation ~
Liaison Psychiatry and Psychosomatic Medicine, New

Orleans. Contact: Academy of Psychosomatic Medicine, 5824 N
Magnolia, Chicago, IL 60660; (312)784-2025.

November 19-20

American Society of Anesthesiologists Workshop on
Obstetrics, Kansas City, Missouri. Contact: ASA, 515 Busse
Hwy, Park Ridge, IL 60068.

December

December 2-4

Ninth Annual Perinatal Postgraduate Course, Jackson,
Mississippi. Sponsored by the University of Mississippi
School of Medicine. Contact: University of Mississippi
Medical Center, 2500 North State St, Jackson, MS 39216-4505;
(601)984-1300.

December 3-6

Workshop in Reconstructive Surgery of the Hand, New

York. Sponsored by the American Society for Surgery of the
Hand. Contact: Terri Harrington, American Society for
Surgery of the Hand, 3025 South Parker Rd, Suite 65, Aurora,
CO 80014; (303)755-4588.

December 4-5

Child Development Course, New Orleans. Sponsored by
Alton Ochsner Medical Foundation. Contact: Ochsner Of-
fice of Continuing Medical Education and Alumni Affairs,
1516 Jefferson Hwy, New Orleans, LA 70121; (504)838-3702.

December 4-5

Contemporary Concepts in Facial Surgery, The Waldorf
Astoria Hotel, New York. Sponsored by Manhattan Eye, Ear
and Throat Hospital in conjunction with The Institute of
Reconstructive Plastic Surgery of the New York University
Medical Center. Contact: Francine Leinhardt, Course Coor-
dinator, Manhattan Eye, Ear and Throat Hospital, 210 East
64th Street, New York, NY 10021; (212)838-9200 ext 2776.

December 4-6

Reconstructive Surgery of the Hand, Valhalla, New York.
Sponsored by American Society for Surgery of the Hand.
Contact: American Society for Surgery of the Hand, 3025
South Parker Rd, Suite 65, Aurora, CO 80014; (303)755-4588.

JOURNAL VOL 140 JULY 49

PROFESSIONAL LISTINGS

THE FERTILITY INSTITUTE OF NEW ORLEANS

(A Professional Corporation)

Richard P. Dickey, MD, PhD

Diplomate, American Board of
Reproductive Medicine
Diplomate, American Board of
Obstetrics and Gynecology

Steven N. Taylor, MD

Diplomate, American Board of
Obstetrics and Gynecology

David N. Curole, MD

Diplomate, American Board
of Obstetrics and Gynecology

Phillip H. Rye, MD

Diplomate, American Board
of Obstetrics and Gynecology

Terry Olar, PhD

Director, InVitro Laboratory
Member, Society for the
Study of Reproduction

REFERRALS ACCEPTED FOR IN VITRO FERTILIZATION
AND OTHER INFERTILITY THERAPY INCLUDING:

MAIN OFFICE

6020 Bullard Ave
New Orleans, LA 70128
(504) 246-8971
(504) 246-8795

SLIDELL OFFICE

700 Gause Blvd
Suite 101
SlideU, LA 70458

UPTOWN OFFICE

2633 Napoleon Ave
Suite 805

New Orleans, LA 70115

TOURO INFIRMARY'S CENTER FOR CHRONIC PAIN

AND

DISABILITY REHABILITATION

1401 Foucher St
New Orleans, LA 70115
(504) 897-8404

Richard H. Morse, MD

Medical Director

Jackie Chauvet

Liaison Coordinator

Elizabeth Messina, RN

Unit Supervisor

50 JOURNAL VOL 140 JULY

' i

JOURNAL

OF THE LOUISIANA STATE MEDICAL SOCIETY August 1988

^ 1 % ^ 0 ^ 3 .
3fS^^ tx: CP^^

yit

'XP^

Louisiana

Physicians

Insurance Agency, inc

A Wholly Owned Subsidiary of LAMMICO

SPECIALLY PRICED PRODUCTS OFFERED:

• Exclusive Physicians Office Package

• Dividend Potential

• Disability Income Protection

• YOU define YOUR medical specialty under definition of
disability

• Additional 15% annual discount to LAMMICO insureds

• Prestige Homeowners Program

• Personal Umbrella

• 111 Veterans Memorial Blvd., Suite 1700 •

• Metairie, Louisiana 70005 •

• ( 504 ) 837'3257 • 1 - 800 - 331-5777 •

A COMMITMENT TO SERVE THE LOUISIANA PHYSICIAN

EDITOR

CONWAY S. MAGEE, MD

CHIEF EXECUTIVE OFFICER
DAVE TARVER

GENERAL MANAGER
RENE ABADBE

MANAGING EDITOR
BONNIE L. BLUNDELL

ADVERTISING SALES
CHARLOTTE SPOONER

JOURNAL COMMITTEE

Chairman, CONWAY S. MAGEE, MD
A.G. KLEINSCHMIDT JR, MD
PAUL F. LARSON, MD
W. CHARLES MILLER, MD
EMILE K. VENTRE JR, MD

Ex officio, DANIEL H. JOHNSON JR, MD

EDITORIAL BOARD

KENNETH B. FARRIS, MD
RODNEY C. JUNG, MD
CONWAY S. MAGEE, MD
W. CHARLES MILLER, MD
ELI SORROW, MD
CLAY A. WAGGENSPACK JR, MD
WINSTON H. WEESE, MD
PATRICK W. PEAVY, MD

EXECUTIVE COMMITTEE

DANIEL H. JOHNSON JR, MD
MILTON C. CHAPMAN, MD
JOHN C. COOKSEY, MD
JAMES W. VILDIBILL JR, MD
SAMUEL A. LEONARD, MD
R. BRUCE WILLIAMS, MD
HOWARD A. NELSON JR, MD
RONALD J. FRENCH, MD
FRANK J. GEORGE, MD
PHILIP A. ROBICHAUX JR, MD
JAMES R. BERGERON, MD
DAVID M. WALSWORTH, MD
CHARLES D. BELLEAU, MD
G. MICHAEL KENT, MD
LEO L. LOWENTRITT JR, MD
EMILE K. VENTRE JR, MD
STANFORD A. OWEN, MD
WALLACE H. DUNLAP, MD

VOLUME 140 / NUMBER 8 / AUGUST

ARTICLES

Barry D. Swartz, PhD
Larry Murray
Betty Alexander, MSW
Frank R. Kauders, MD
Don Gallant, MD

The cocaine epidemic:
Drug abuse patterns in
New Orleans

Francis A. Puyau, MD

Needle localization of
occult breast cancer for
surgical biopsy

Don M. Morris, MD
Kenneth Robbins, MD

The effect of method of
biopsy and timing of
mastectomy on the
development of post
mastectomy nosocomial
wound infection

Established 1844. Owned and edited by The
Journal of the Louisiana State Medical Society, Inc,
1700 Josephine St, New Orleans, LA 70113.

Subscription price is $12 per year in advance,
postage paid for the United States; $15 per year for
all foreign countries belonging to the Postal Union;

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Advertising: Contact Charlotte Spooner, 1700
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The JOURNAL (ISSN 0024-6921) is published
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and additional mailing offices.

Articles and advertisements published in the
JOURNAL are for the interests of its readers and do
not represent the official position or endorsement
of The Journal of the Louisiana State Medical Society,
Inc or the Louisiana State Medical Society. The
JOURNAL reserves the right to make the final
decision on all content and advertisements.

DEPARTMENTS

2 Information for Authors

3 Viewpoint

5 New Members

7 ECG of the Month

11 Otolaryngology/Head

& Neck Surgery Report
15 Auxiliary Report

19 Medical Student Section

26 Calendar

49 Classified Advertising

Cover illustration by Eugene New, New Orleans

INFORMATION FOR AUTHORS

The JOURNAL welcomes material for publication if submitted by a
Louisiana physician in accordance with the following guidelines. Ad-
dress all correspondence to the Editor, Journal of the Louisiana State
Medical Society, 1 700 Josephine Street, New Orleans, LA 701 13. Con-
tact the managing editor with any questions concerning these guidelines
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TITLE PAGE should carry [1 J the title of the manuscript, which should
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JOURNALS

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PATIENT DIGNITY, PHYSICIAN DIGNITY,
AND MEDICAL EDUCATION

I N PAST Viewpoint articles, we have
argued that the preservation of
patient dignity is the central ethic
of the medical profession. We fur-
ther posited that present profes-
sional behavior indicates that we
have lost sight of that benchmark.
One reason may be the inordinate
amount of time medical students
are required to devote to the study
of the sciences. Little time is left in
the curriculum to discuss issues of
morality. The neophyte is left be-
lieving that a competent physician
is one who need only know what
therapeutic medical modalities are
possible but not the one which is
morally acceptable. We would like
to suggest another, but related,
reason why medical education is
doing a disservice to our profes-
sion and society.

The relationship between the
patient and physician is a cove-
nant. Under this biblical concept,
a person in whom another person
has placed a special trust or con-
fidence is required to act in good
faith and in the interests of the per-
son reposing that trust or confi-
dence. Furthermore, the agree-
ment is timeless: it changes forever
the lives of those who enter into
the covenant. The critical nature of
the issue between patient and phy-
sician, patient self-worth, de-
mands an unwavering, enduring
fidelity to this trust.

In being faithful to that trust,
a physician may deny a patient a

requested service. For example, a
woman and her husband may seek
an abortion. The pregnancy is ac-
cidental and unwanted. Their sense
of self-worth is threatened by the
anticipated, imperious control of
their lives by the baby. They seek
relief from a physician. He refuses
to provide the service. Assuming
he is competent to perform the sur-
gery, and they are rational, the
physician may give one of two ex-
planations for his decision: to per-
form the surgery would be to deny
his right to defend his moral prin-
ciple of the sanctity of human life,
or to perform the surgery would
be to deny the trust placed in him
by the patient, which now is the
fusion person of mother and fetus.

We maintain that the latter is
a more valid argument. The action
correctly flows from a concern for
the welfare of the patient. That the
physician chose to value the prin-
ciple of not killing more highly than
the principle of parental autonomy
is unimportant. He acted in concert
with his moral charge: to defend
the dignity of the patient.

The former reason, though
teleologically identical, is flawed by
its intent. Here the physician's ac-
tion is spawned by a defense of his
principles and his autonomy. Un-
less the patient and his physician
can agree on moral intent, their ac-
tions may be discordant. For ex-
ample, an opera singer with laryn-
geal cancer refuses surgical

extirpation although it offers better
survivability and chooses chemo-
therapy because he values his life
with a voice more highly than
without it. His physician insists that
his patient choose surgery which
reflects his moral imperative to
preserve life and to proscribe what
he thinks is suicide. Without con-
sidering the long-held principles
which his patient is reflecting upon,
the physician may be doing his pa-
tient a disservice. When con-
fronted by conflicting principles,
the physician is not always justi-
fied in choosing his own.

In this conflict, by sacrificing
his principles and autonomy, the
patient will almost always lose
more. The patient consults the
physician because he feels less
worthy and seeks a remedy. By de-
fending his patienf s principles and
autonomy, the physician has be-
gun to effect healing. The physi-
cian wUl have signaled to his pa-
tient that though ill, he is still a
person of full value. To do other-
wise, would further damage the
patient's self-image and would
fracture the covenant.

The physician has very little to
lose. He is the dominant partner in
the covenant. He is not in need; he
is the needed. He stands to gain
through the satisfaction of know-
ing he has helped and through re-
muneration. His power will not be
effaced by placing the importance
of his moral needs below those of ►

JOURNAL VOL 140 AUGUST 3

his patients. In fact, his healing ef-
fect will be enhanced, and he will
have acted in concert with the spirit
of the covenant. Many fourth-year
medical students we teach are un-
aware of or unwilling to consider
this argument. Part of the problem
may lie with medical education.

Students report that it is not
uncommon for instructors to be ill-
prepared, to read their presenta-
tions to the class, to be late or to
fail to appear without notice, to
teach by intimidation, to repri-
mand before a group, and to fail to
compliment. They have also wit-
nessed curt, insensitive, and dif-
ferential care given to patients by
attendings, questionable care to
save time, and lying on rounds by
house officers to preserve reputa-
tion. This callous disregard for stu-
dent dignity and for the quality of
professional behavior witnessed by
the student has a malignant effect
on the care these students will of-
fer.

Medical students and house
officers spend the major part of
seven to 10 years becoming phy-
sicians. They irrationally perceive,
because of the duration and inten-
sity of the educational experience,
that their self-worth is tantamount
to their success as a student phy-
sician. They forget that, morally, a
person has inestimable, unchang-
ing value. They forget, too, that
though parts of our personhood
may be damaged, they heal; or if
permanently mutilated, other ac-
tivities can be substituted to fully
reconstitute our self-perception of
worth. It is possible, though, that
after repeated deprecation for ex-
tended periods during times of
continuous stress, the student fi-
nally may believe that he is less
worthy.

Although the education of a
physician is less than scientific, one
method has repeatedly been
proved to be most valuable in de-

While educating stu-
dent physicians, it is im-
portant for teachers not
oniy to share by word and
exampie the importance
of patient dignity, but to
safeguard the dignity of
their students as weii.

veloping desirable behavior in stu-
dents: the role model. It is by living
the ideal professional life that
teachers can most efficiently teach
their students. If teachers consist-
ently demonstrate that dignity is
unimportant to all but the physi-
cian, this, too, may be learned.

The importance of these ef-
fects becomes more evident when
the analogy between the physi-
cian-patient and the teacher-stu-
dent relationship is perceived: be-
cause these relationships are
concerned with the neverending
processes of nurturing and growth,
both are covenants.

The rules governing the per-
sonal behavior of the dominant ac-
tor in a covenant are learned by the
student during his apprenticeship
years, and they are transferred to
the professional behavior of his
mature years. True, he has been
exposed to these principles in his
passage to adulthood but never
while in this moral position.

In his private life, a physician
has the freedom of any citizen to
order the hierarchy of his princi-
ples of moral action, but as phy-
sician qua physician he is severely
constrained by the covenant. The
dual and sometimes disparate ex-
istence of a physician, involving his
duties as a citizen and his duties of
station, frequently is not appreci-

ated. Some duties which may have
been optional become mandatory.
For example, society does not re-
quire benevolence from its mem-
bers; it only requires us to refrain
from malevolence. While we are
not required to put a dollar in a
beggar's cup, we are constrained
from kicking him in the skins. As
the dominant partner in a medical
or teaching covenant, physicians
are required to do good. Also, as
previously illustrated, circum-
stances may even require that phy-
sicians and teachers value patient
and student principles above their
own.

A physician's work is de-
manding. Besides remaining cur-
rent with a rapidly expanding lit-
erature and devoting long hours to
caring, he must accept the prem-
ises that sacrifices of moral prin-
ciples are required in the service of
patient dignity and that such sac-
rifices are not demeaning.

To consider these premises,
the student first must know of
them. To accept them and to act,
the student must have a firm faith
in the goodness of the action and
in himself. Therefore, this knowl-
edge must come through sincere,
convincing, and compassionate
education. While educating stu-
dent physicians, it is important for
teachers not only to share by word
and example the importance of pa-
tient dignity, but to safeguard the
dignity of their students as well.
Otherwise, we are left with un-
educated and insecure physicians
who either do not know that they
should, or if they do, are afraid to
act on behalf of patient dignity. ■

IRWIN COHEN, MD
CAROLYN ROBERTS

4 JOURNAL VOL 140 AUGUST

NEW MEMBERS

Applications for membership have been re-
ceived from the following physicians by the
respective parish medical societies as of May
4, 1988. The Loxiisiana State Medical Society
is pleased to welcome:

■ East Baton Rouge

Charlie H. Bridges, MD

7777 Hennessy Blvd #608, Baton Rouge
70808

1978, University of Mississippi School of
Medicine
urology

Gregory O. Harrison, MD

1770 Physicians Park Dr, Baton Rouge
70816

1980, Tulane University School of
Medicine
general surgery

■ Jefferson

David W. Hoemer, MD

4315 Homna Blvd, Metairie 70006

1983, Louisiana State University School of
Medidne, New Orleans

obstetrics & gynecology

■ Morehouse

Charles W. Mason, MD

420 Gunby, Bastrop 71220

1984, Louisiana State University School of
Medidne, New Orleans

internal medicine

Richard D. Nichols, MD

512 S Washington, Bastrop 71220
1973, University of Iowa College of
Medidne
orthopedic surgery

Robert M. Raulerson, MD

323 W Walnut, Bastrop 71220

1985, University of Miami School of
Medidne

emergency medicine

■ Natchitoches

Fred M. Sullivan Jr, MD

617 Bienville St, Natchitoches 71457
1982, Louisiana State University School of
Medidne, New Orleans
pediatrics

■ Orleans

Claremont F. Carter, MD

1542 Tulane Ave, New Orleans 70112
1976, Facultad de Medidna de la
Universidad de Salamanca, Spain
diagnostic radiology

Bruce G. Combs, MD

3500 St Charles Ave, New Orleans 70115

1980, University of Utah College of
Medidne

internal medicine

David L. Sommerville, MD

PO Box 19024, New Orleans 70179
1968, University of Pennsylvania School
of Medidne
diagnostic radiology

■ Ouachita

Jose M. Marina-Cortes, MD
1910 Jackson St, Monroe 71211
1965, University of Puerto Rico School of
Medidne
general practice

WUlilam H. Matthews, MD

1900 N Seventh, West Monroe 71291
1982, Louisiana State University School of
Medidne, Shreveport
internal medicine

■ River Parishes

Louise M. Becnel, MD

1028 S CarroUton #3, New Orleans 70118
1984, Louisiana State University School of
Medidne, New Orleans
internal medicine

■ St Tammany

Ernest E. Martin Jr, MD

2810 Rorida, MandeviUe 70448

1981, Louisiana State University School of
Medidne, New Orleans

family practice

James H. Newcomb, MD

1340 14th St, SHdeU 70458
1984, Louisiana State University School of
Medidne, New Orleans
family practice

■ Shreveport

Johnny B. Craig, MD

846 Margaret PI, Shreveport 71101

1980, Louisiana State University School of
Medidne, Shreveport

oncology

Harry R. Parvey, MD

PO Box 33932, Shreveport 71130
1977, Medical College of Wisconsin
diagnostic radiology

Kalia K. Sadasivan, MD

1501 Kings Hwy, Slueveport 71130
1974, Facultad de Medidna de la
Universidad Nadonal de Colombia
orthopedic surgery

William A. Sodeman Jr, MD

1501 Kings Hwy, Shreveport 71130
1960, University of Pennsylvania School
of Medidne
internal medicine

■ Terrebonne

Robert K. Gamble, MD

1350 W Tunnel Blvd #6C, Houma 70360

1981, Universidad Nordestana, Dominican
Republic

hematology

Herminio Suazo-Vasquez, MD
1350 W Tunnel Blvd #21, Houma 70360
1973, Facultad Ciendas Medicas,
Universidad Autonoma de Honduras
internal medicine

■ Webster

David L. Shepard, MD

Two Medical Plaza, Minden 71055
1981, College of Medicine University of
the East, Philippines
internal medicine

Robert M. Walker, MD

10270 EUerbe Rd, Shreveport 71106
1981, Louisiana State University School of
Medidne, Shreveport
radiology

JOURNAL VOL 140 AUGUST 5

■ IntemI Resident Members

EAST BATON ROUGE

David L. Cunningham, MD

4727 W Park Dr, Zachary 70791
1982, Louisiana State University School of
Medicine, New Orleans
urology

David E. Harper, MD

5825 Airline Hwy, Baton Rouge 70805
1987, Louisiana State University School of
Medicine, New Orleans
family practice

Ron D. Waldrop, MD

16749 Dahgren Dr, Baton Rouge 70817
1987, University of Texas Medical School
pediatrics

JEFFERSON

Steven F. Freedman, MD

636 Stratford Dr, Harahan 70123
1985, Tulane University School of
Medicine
otolaryngology

ORLEANS
Felix P. Bopp, MD

523 Dumaine St #3, New Orleans 70116

1984, Tulane University School of
Medicine

otolaryngology

Martin D, Gray, MD

1415 Tulane Ave, New Orleans 70112
1983, Rush Medical College
psychiatry

Paul T. Le, MD

2411 Richland #302, Metairie 70001
1987, Case Western Reserve University
School of Medicine
general surgery

Mark D. Smith, MD

1542 Tulane Ave, New Orleans 70112

1985, Louisiana State University School of
Medicine, New Orleans

obstetrics & gynecology

Vashu D. Thakur, MD

1415 Tulane Ave, New Orleans 70112
1976, Topiwala National Medical College,
India
nephrology

Mark W. Valentine, MD

1430 Tulane Ave, New Orleans 70112
1983, Tulane University School of
Medicine
general surgery

Sarah V. Webb, MD

1430 Tulane Ave, New Orleans 70112
1985, Tulane University School of
Medicine
pathology

OUACHITA

Anup J. Giokli, MD

1602 Erin St, Monroe 71201
1980, University of Bombay, India
family practice

SHREVEPORT

Jason E. Edling, MD

1501 Kings Hwy, Shreveport 71130
1985, University of Texas Medical Branch,
Galveston
internal medicine

ofWV South

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(318) 632-5111 In Shreveport

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(Opening Oct. 1, 1988)

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6 JOURNAL VOL 140 AUGUST

ECG OF THE MONTH

TRIUMVIRATE

JORGE I. MARTINEZ-LOPEZ, MD

The rhythm strip shown below was recorded on a modified, bipolar chest lead, with the positive electrode
in the precordial V5 position. It was recorded in the CCU from a patient suspected of having acute
myocardial infarction. No other details are available.

What is your diagnosis? Elucidation is on page 8.

JOURNAL VOL 140 AUGUST 7

ECG of the Month

Case presentation is on page 7.

DIAGNOSIS — To be discussed

Even the most inexperienced of interpreters should
be able to notice that the rhythm strip displays three
different ECG events in a very brief period. The sig-
nificance of these electrical events is the subject of the
discussion to follow.

DISCUSSION

The first segment of the rhythm strip consists of six
cardiac cycles, each containing a P-QRS-T sequence.
The P waves, depicting biatrial depolarization, are
clearly of sinus origin and recur regularly at 79 times
a minute. Peaking of the sinus Ps suggests atrial pa-
thology. Each sinus P is followed by a narrow QRS
complex, after a normal PR interval. These two find-

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ings indicate that both atrioventricular and biventric- I
ular conduction are of normal duration, and that the
ratios of atrial to ventricular responses are 1:1. Also
of normal duration is the QT interval, a measurement
of the total duration of electrical ventricular systole.
On the other hand, ventricular repolarization is ab- |
normal as evidenced by the diphasic T waves. In sum-
mary, the first six cardiac cycles are sinus in origin,
with 1:1 A:V ratios, normal PR, QRS, and QT inter- |
vals, and abnormal T waves.

After the sixth sinus cycle, changes take place:
seven abnormally-wide QRS complexes appear ab- !
ruptly and recur at rapid rates (tachycardia) . The pres-
ence of wide QRS tachycardia requires determination S
of its origin, ie, supraventricular versus ventricular. |
For wide QRS tachycardia to occur in response to j
supraventricular impulses, the impulses have to be !
conducted into the ventricles aberrantly, in the pres- [
ence of preexisting bundle branch block, or by way
or one or more accessory pathways. Alternately, wide
QRS tachycardia may be secondary to reentry, en-
hanced automaticity, or triggered activity in the ven-
tricle.

ECG findings that favor a ventricular origin for
wide QRS tachycardia include: AV dissociation, in-
termittent normalization or fusion of the QRS com-
plexes (Dressler's beats), a QRS duration greater than
140 m/sec, left axis deviation in the frontal plane, and
certain configurations displayed by the QRS com-
plexes. In the tracing shown here, the search for clues
is limited because only a single lead is available for
analysis. It will be noted that the first wide QRS of
the short burst of tachycardia is followed by a sinus
P, superimposed on its ST segment; this identifies the
first wide QRS as a ventricular premature complex.
Because the six wide QRS complexes that follow the
first one have similar morphologies, one can conclude
that these, too, are ventricular, and that the short
burst represents a nonsustained episode of mono-
morphic ventricular tachycardia. The exact electro-
physiological mechanism responsible for the nonsus-
tained ventricular tachycardia can not be stated with
certainty. However, because the short burst is slightly
irregular and ''warms up" to a rate of 150 a minute
before it ends abruptly, enhanced automaticity of a
ventricular focus is favored over reentry as the elec-
trophy siological mechanism.

In the search for AV dissociation in wide QRS
tachycaradia, sinus and ventricular impulses must be

8 JOURNAL VOL 140 AUGUST

, independent of each other. It was already established

I that the first wide QRS of the nonsustained tachy-
cardia was “dissociated." However, if calipers are set
I to the sinus P-P cycle, no other sinus Ps can be iden-
tified "marching" through the paroxysm. This finding
suggests that the sinus cycles have been disturbed by
j the ventricular tachycardia, most likely as a result of
retrograde VA conduction, which is a common oc-
' currence. Retrograde P waves are not clearly visible
diiring the short burst of ventricular tachycardia either,

1 but they may be responsible for the peaking of the T
waves.

The nonsustained episode of ventricular tachy-
cardia races to its own extinction and ends as abruptly
as it started. After a brief interlude, during which
sinus Ps fail to emerge, a third set of events develops.
This last sequence is characterized by the sudden ap-
pearance of narrow QRS complexes, recurring regu-
larly at rates of 135 times a minute. The configuration
of the narrow QRS complexes is identical to those
recorded during sinus rhythm; but, in contrast to the
earlier ones, sinus Ps do not precede them. Instead,
inverted P waves follow each narrow QRS complex
with short R-P Intervals. The characteristics of this
narrow QRS tachycardia is consistent with the diag-
nosis of the common type of AV nodal reentry tach-
ycardia. Thus, AV nodal reentrant tachycardia ab-
ruptly replaces the now extinct ventricular tachycardia.
The possible mechanism responsible for the electro-
physiological swap is not clear.

The tracing, therefore, is Interesting because of
the triumvirate it shows, occurring in a very brief
period in the same patient. The triumvir consists of
sinus rhythm, nonsustained monomorphic ventric-
ular tachycardia, and AV nodal reentrant tachycardia,
each successful at different times in controlling the
cardiac rhythm. ■

SELECTED REFERENCES

1. Wellens HJ, Barr FWHM, Lie KI: The value of the electrocardiogram in
the differential diagnosis of a tachycardia with a wide QRS complex. Am
J Med 1978;64:27-33.

2. Morady F, Scheiiunan MM, Hess DS: Mechanism and management of
parox)'smal supraventricular tachycardia. Cardiaoasc Rev & Rep 1981;2:1014-
1038.

3. Bar FW, Brugada P, Dassen WR, et al: Differential diagnosis of tachycardia
with narrow QRS complex (shorter than 0.12 second). Am J Cardiol
1984;54:555-560.

4. German LD, Ideker RE: Ventricular tachycardia. Med Clin North Am
1984;68:919-934.

5. Akhtar M: Atrioventricular nodal reentrant tachycardia. Med Clin North
Am 1984;68:819-830.

Dr Martinez-Lopez is a specialist in cardiovascular diseases affiliated
with the Cardiology Service, Dept of Medicine at William Beaumont
Army Medical Center in El Paso, Texas.

The opinions and assertions contained herein are the private views of the
author and not to he construed as official or as reflecting the views of
the Dept of the Army or Dept of Defense.

Reprints will not be available.

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JOURNAL VOL 140 AUGUST 9

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JOURNAL VOL 140 AUGUST

PHOTOGRAPHY COURTESY OF SIEMENS MEDICAL SYSTEMS, INC.

OTOLARYNGOLOGY/

HEAD & NECK SURGERY REPORT

SARCOIDOSIS AND SARCOIDOSIS OF

THE LARYNX

RONALD E. JAMERSON, MD; PAUL A. BLAIR, MD

Sarcoidosis is a multisystem granulomatous
disease of undetermined etiology, most commonly
involving the lungs but on rare occasions
involving the larynx. A review of the medical
literature shows that the supraglottic region of the
larynx is most commonly involved, and that
symptoms of airway obstruction are more common
than hoarseness. Unless severe airway problems
exist, the disease can be managed expectantly. If
airway obstruction symptoms become severe,
treatment may range from systemic steroids,
intralesional steroids, or local excision to

tracheotomy.

S arcoidosis is a multisystem granulomatous dis-
ease of undetermined etiology, most frequently
presenting with bilateral hilar adenopathy, pulmo-
nary infiltration, and eye or skin lesions. Although
the disease has an increased affinity for the reticu-
loendothelial system, occasionally patients may pres-
ent with symptoms and lesions that fall within the
realm of otolaryngology/head and neck surgery. Those
areas most frequently seen and written about include
the nose, tonsils, larynx, parotid gland, and cranial
nerves. This paper will discuss sarcoidosis of the lar-
ynx and its treatment.

The disease was first described clinically by Jon-
athan Hutchinson in 1869. However, it was not until
1899 that Caesar Boeck^ described the histological ap-
pearance of the cutaneous lesions. Sarcoidosis has a
general worldwide distribution. The highest preva-
lence rate is in Scandinavia where 64 of 100,000 per-
sons were found to have pulmonary manifestations.^
Sarcoidosis also is more prevalent in the southern
parts of the United States, and has a male to female
ratio of 1:2, and a black to white ratio of 10:1. The
disease is most commonly found in persons in the
third and fourth decades of life.^

JOURNAL VOL 140 AUGUST 11

PATHOGENESIS

As the definition states, the pathogenesis of sar-
coidosis remains a mystery. There appears to be a
host response to an unknown stimulus, probably an
infectious agent; but possibly an autoimmune disease
or one of abnormal immune regulation; or a response
to chemical factors, such as zirconium or beryllium.'’
Reduced lymphocyte blastogenesis, circulating im-
mune complexes and the inability to develop and
maintain delayed-type hypersensitivity are common
features. In short, cell mediated immunity is dimin-
ished, and will be manifested by negative results in
skin test to various antigens such as mumps, Candida,
and tuberculin. The humoral immunity is heightened
as evidenced by the hypergammaglobulinemia which
is seen frequently in sarcoidosis.'’

PATHOLOGY

The pathologic hallmark of sarcoidosis is the presence
of noncaseating granulomas of the involved organs
or tissue. Epithelioid cells and giant cells of the foreign
body and Langhans' type make up the granuloma.
Intracytoplasmic inclusion bodies such as Schau-
mann's and asteroid bodies are also commonly seen,
but are not pathognomonic for sarcoidosis. Therefore,
cultures and special staining techniques are needed
to rule out fungal diseases, leprosy, tuberculosis, and
berylliosis as the cause of the granulomas.^

CLINICAL FEATURES

The diagnosis of sarcoidosis is made on the basis of
clinical features such as fever, weight loss, malaise,
arthralgia, lymphadenopathy, cough, or dyspnea;
noncaseating granulomas of involved organs or tis-
sues; a positive Kveim test; positive chest x-ray find-
ings; and blood studies. Although a majority of sar-
coid patients have a negative reaction to several skin
tests, 50-80% will respond to an intradermal injection
of antigen extracted from the spleen or lymph node
of known sarcoid patients. A papule will appear 4-6
weeks after injection, with the biopsy of the papule
showing noncaseating granuloma. There are two
problems that exist with this Kveim test: 1-2% false
positive rates are seen, and 50% of the patients fail
to react to the antigen 5 years after the onset of the
disease.^

Certain blood studies are frequently abnormal. A

total of 50-75% of the patients show an increase glob-
ulin level in the serum. A total of 20% of the patients
are hypercalcemic and 50% may have elevated liver
enzymes. Also, eosinophilia has been found in 20%
of sarcoid patients.^ Serum angiotensin-converting
enzyme is also elevated in patients with sarcoidosis,
with the level paralleling the course of the disease.’'

Although any organ system may be involved in
sarcoidosis, the lungs are the most frequently af-
fected; 88% of sarcoid patients having an abnormal
chest x-ray. Various stages of sarcoidosis have been
classified. Those patients with normal chest x-rays are
classified as stage 0. Stage I will reveal bilateral hilar
adenopathy only on the chest film and is found in
51% of patients with sarcoidosis. A total of 60% of
these patients will undergo spontaneous remission.

A total of 31% will have stage 11 pulmonary disease; i
described as having pulmonary infiltration combined
with the hilar adenopathy. Stage III, where the pul-
monary infiltrate persists but the hilar adenopathy
has disappeared, is found in only 6%. Only 12% cf
the patients will have remission of their disease, while
the remainder develop nonreversible pulmonary fi-
brosis.'

LARYNGEAL MANIFESTATIONS I

Of particular interest to the otolaryngologist is the
patient with sarcoidosis who may present with lar-
yngeal involvement. Laryngeal involvement is rela-
tively uncommon, occurring in 1-5% of the patients
who are diagnosed with sarcoidosis. “ All or any part
of the larynx may be affected, with the pathology of
the larynx varying from diffuse or localized edema to
a solid mass resembling a tumor. Ulceration is a rare
occurrence because the disease process is submu-
cosal.*'

When sarcoidosis does involve the larynx, the
pathology usually has a predilection for the supra-
glottic area. Neel and McDonald® looked at 13 patients
with laryngeal sarcoidosis, representing a small per-
centage of 2,319 patients with sarcoidosis seen at the
Mayo Clinic from 1950 through 1981. Eleven of their
13 patients had involvement of the supraglottic region
and only two had involvement of the subglottic lar-
ynx. They commonly found, on direct laryngoscopy,
a diffuse, pale, edematous supraglottic structure which
they considered to be pathognomonic.® The true vocal
cords are rarely involved probably because of the

12 JOURNAL VOl, 140 AUGUST

scarcity of lymphatics in the region of the larynx.^ The
histologic appearance of the laryngeal lesion is the
same as seen in other locations of sarcoidosis: non-
caseating granulomas, composed of epithelioid cells
and giant cells.

When the lesion begins to cause problems, air-
way obstruction is usually the primary symptom. Be-
cause these lesions do not ulcerate, pain and he-
moptysis are uncommon findings. Hoarseness is
another complaint with which the patient may pre-
sent, but this finding is also rare because vocal cord
involvement is infrequent.

TREATMENT

The treatment of sarcoidosis follows no specific guide-
lines. Because the disease has a tendency toward
spontaneous regression, patients presenting with only
mild to moderate airway symptoms may be treated
expectantly by periodic examinations. However, when
a severe airway problem occurs, high dose steroids
given systemically or by local injection have seemed
to relieve some of the initial swelling.^ Chloroquine,
with its anti-inflammatory properties, has also been
shown to be beneficial in the treatment of these pa-
tients. Other patients have received symptomatic re-
lief with local excision of the sarcoidosis. Many of
these patients have undergone tracheotomies for air-
way management until the disease process regressed
spontaneously or with the use of steroids.

In general, systemic steroids are recommended
for the treatment of active ocular disease, persistent
hypercalcemia, central nervous system disease, my-
ocardial involvement, progressive pulmonary dis-
ease, and impending laryngeal obstruction.^ There
have also been rare cases of laryngeal sarcoidosis
treated with radiation therapy,^' but many feel the
failures outnumber the successes, and the potential
hazards of radiation therapy limit its usefulness in
laryngeal sarcoidosis.

CONCLUSION

Sarcoidosis is a multisystem granulomatous disease
of unknown etiology which can on occasion involve
the larynx. The diagnosis may be made by a combi-
nation of clinical evaluation, histological examination
of involved tissue, cutaneous anergy, positive Kveim
test, and certain abnormal laboratory or radiographic

findings. When presented with a patient with upper
airway obstruction, the physician should include sar-
coidosis in the differential diagnosis of lesions in-
volved in this area.

REFERENCES

1. Miglets AW, Vial JH, Kataria YP, et al: Sarcoidosis of the head and neck.
Laryngoscope 1977;87:2038-2048.

2. Bauer JH, Lofgren S: International study of pulmonary sarcoidosis in
mass chest radiography. Acta Med Scand 1964;1076(suppl 425):103.

3. Johns CJ: Sarcoidosis: Harrison's Principles of Internal Medicine, ed 9. New
York, McGraw-Hill Book Co, 1980.

4. Mitchell DN, Scadding JG: Sarcoidosis. Am Rev Respir Dis 1974;110:774-
802.

5. Neel HB, McDonald TJ: Laryngeal sarcoidosis. Ann Otol Rhinol Laryngol
1982;91:359-362.

6. Casuccio JR, Yanagisawa E: Diseases of obscure etiology; Sarcoidosis,
Wegener's granulomatosis, and Midline granuloma. Otolaryngol Clin North
Am. 1981;14(2):331-345.

7. DeRemee RA, Rohrbach MS: Techniques in evaluation of sarcoidosis.
Semin Respir Infect 1981;3:54-56.

8. Devin KD: Sarcoidosis and sarcoidosis of the larynx. Lan/ngoscope
1965;75:533-569.

9. Weisman RA, Canalis RF, Powell WJ: Laryngeal sarcoidosis with airway
obstruction. Ann Otol Rhinol Laryngol 1980;89:58-61.

10. Morse SI: The treatment of sarcoidosis with chloroquine. Am } Med
1961;30:779-784.

11. Carasso B: Sarcoidosis of the larynx causing airway obstruction. Chest
1974;65:693-695.

Dr Jamerson is a resident in the Dept of Otolaryngology/ Head and Neck
Surgery at Tulane University Medical Center in New Orleans.

Dr Blair is a professor of otolaryngology/head and neck surgery at
Tulane University Medical Center in New Orleans.

Reprints will not be available.

JOURNAL VOL 140 AUGUST 13

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JOURNAL VOL 140 AUGUST

Jackie Tucker, LSMSA President

AUXILIARY REPORT

TRAINING THE LEADERS OF TODAY

FOR TOMORROW

BEVERLY W. VIDACOVICH

W hat are the characteristics of a good leader? In
Standard Code of Parliamentary Procedure, Alice
Sturgis says:

There are certain fundamental qualities that most good leaders
have in common. One is the ability to plan — to sense what
the members want and to help them crystallize their ideas.
Another is the ability to unite — to rally members behind a plan
and behind their leader. Perhaps the most important is the
courage to win — to overcome all obstacles.

Today, many obstacles are faced by the Auxiliary
and by the medical profession. There is much change
and upheaval and it is more vital now than ever that
the Auxiliary identify, develop, and train its leaders
so they can face the many challenges with which we
are beseiged.

Critical issues like the growing AIDS problem,
adolescent health problems including teen suicide,
teen pregnancy and substance abuse, the abuse of
professional liability, the impaired physician, the in-
trusion of government and private industry and their
attempts to control medicine are but a few of the many
crises we face.

Well-trained leaders are essential for the growth
of any organization, but are especially critical to an

all- volunteer force like the Auxiliary. Effective lead-
ership training is imperative also so that auxilians can
be better prepared to work as a team in an ever in-
creasing role of support to the medical society to fur-
ther the goals and ideals of the medical profession.

How are effective leaders developed and trained?
Leaders are developed not by accident, but by design
and careful planning. Building on an individual mem-
ber's interest, education, and past experience, poten-
tial leaders begin at the parish level and are system-
atically put into higher and higher positions of
responsibility. Leadership training programs for
members are developed through a special team — the
AMA Auxiliary federation of national, state and par-
ish auxiliaries.

At the national level, two leadership confluence
meetings are held annually for state and parish lead-
ers to provide intensive leadership training. These
leaders have the opportunity at Confluence to interact
and consult with other auxilians at all levels on im-
portant areas such as communications, effective pro-
gramming, finances, and building membership.
Speakers selected for their expertise provide infor-
mation and educational experiences on topics dealing ►

JOURNAL VOL 140 AUGUST 15

with legislative issues, health issues such as AIDS,
adolescent health and community action against
smoking, and medical family support. Participants
may be exhausted by the pace of Confluence but al-
ways return inspired and fired up with enthusiasm
and new ideas. National is also an invaluable source
of resource material and personnel, publications, and
audio-visual materials.

At the state level. Leadership Conference, Mid-
Year Board, and the Annual Convention are designed
to further enhance leadership development. These
meetings provide auxilians throughout the state with
an excellent source of inspiration, information, and
interaction with other members.

Leadership Conference held annually with the
LSMS provides leadership training through outstand-
ing speakers in such areas as legislation, health proj-
ects, membership, and other important issues that
affect the medical profession and the auxiliary.

At Mid-Year Board, workshops, training ses-
sions, and speakers are selected to inform, educate.

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and develop skills such as public speaking for auxil-
iary members.

Mid-Year Board and the Annual Convention also
provide a forum to apprise members of the business
and projects of the Auxiliary.

At the parish level, auxiliary members receive
important initial "on-the-job training" by serving as
officers and working on various committees and
events, in addition to the other activities planned by
parish auxiliaries to educate and train their members
and to develop their individual skills. It is at this first
level of auxiliary involvement that the development
of potential future leaders begins.

The future of the Auxiliary depends upon the
training of these leaders if we are to effectively con-
tinue to promote the goals of the medical profession,
meet community health needs, and provide support
for the medical family. Participation on as many levels
of leadership training as possible by physician's
spouses must be encouraged to help insure the ful-
fillment of these goals.

Theodore Friend III, past president of Swarth-
more College, made an interesting summation of the
concept of leadership:

Leadership is heading into the wind with such knowledge of
oneself and such collaborative energy as to move others to
wish to follow. The angle into the wind is less important than
choosing one and sticking reasonably to it, which reason-
ability includes willingness to be borne by friendly currents.

Followers do not collect to exhortation, but adhere from
example. In action and in articulation, leading requires that
one know where one is taking oneself; from the being that
has been to the one that wishes to be, despite ambiguities,
and against the odds that inhere in ideals.

It is time for the Auxiliary in conjunction with
the medical society to intensify efforts to develop the
caliber of leaders that will enable us to "head into the
wind" of change and stay on our course of improving
the health and quality of life for all people. ■

Mrs Vidacovich (wife of Richard P. Vidacovich, MD) is president-elect
of the Louisiana State Medical Society Auxiliary.

16 JOURNAL VOL 140 AUGUST

MEDICAL STUDENT SECTION

MEDICAL STUDENT PERSPECTIVES
ON THE LOUISIANA CHARITY
HOSPITAL SYSTEM

FRANK D. GROVES, MD

O UR state's charity hospitals have repeatedly made
the headlines this year, as a new administration
seeks ways of streamlining state government and re-
ducing budget deficits. Louisiana medical students
share the inevitable anxiety as we wait to see where
the budgetary ax will fall next. Few state programs
are as directly tied to medical education as the Charity
Hospital System, for it is in these public hospitals that
most of our clinical training occurs. Thus, we wait
expectantly as Governor Buddy Roemer's reforms take
shape. Often, we feel that we could offer valuable
input into the development of new policies, if only
someone were willing to listen.

Fortunately, the Louisiana State Medical Society
(LSMS) has been willing to listen — in the form of a
brief survey distributed to 600 junior and senior stu-
dents at both New Orleans medical schools in May
1988. This year's survey is limited to students having
contact with "Big Charity" Hospital in New Orleans.
Responses are now being coded for analysis, and the
results should be available by the end of the year.

This is the second year in a row that the LSMS
has surveyed student opinion on the Charity Hospital
System. The first such survey took place in May 1987,

when a more detailed questionnaire was distributed
to 800 students at all three Louisiana medical schools.
(The same questionnaire had previously been used to
survey the House of Delegates in the fall of 1986.^)
Results of the 1987 student survey are reported here,
and will be compared with the responses given by
the House of Delegates.

SAMPLE SIZE AND RESPONSE RATE

Questionnaires were distributed to 811 students, and
145 responses were received (18% response rate). The
responses were divided equally between third- and
fourth-year medical students, representing a broad
spectrum of anticipated specialties. Responses from
all three schools were pooled in evaluating the state
Charity Hospital System as a whole.

A total of 117 replies were received from students
in the Greater New Orleans Area. Responses from
both New Orleans schools were pooled in evaluating
"Big Charity." The response rate at LSU-Shreveport
was somewhat lower, with only 28 replies out of 178
questionnaires mailed (16% response rate). The eval-
uation of Confederate Memorial Hospital (Shreve- ►

JOURNAL VOL 140 AUGUST 19

port) is based on responses from Shreveport students
only.

A total of 19 students representing all three schools
submitted evaluations of Earl K. Long Memorial Hos-
pital (Baton Rouge). Although the results from Earl
K. Long are presented here, they should be viewed
with caution because of the small number of re-
sponses. No other branch hospital received more than
a handful of evaluations.

EVALUATION OF THE
CHARITY HOSPITAL SYSTEM

Respondents were asked a series of essay questions
which were subjected to content analysis. The first
question was "What do you think is the primary jus-
tification for having the Charity Hospital System?" A
total of 77% of the students felt that the primary jus-
tification is to "provide care for the medically indi-
gent." (Of the 1986 House of Delegates, 69% had
given a similar response.) Respondents next were
asked, "Do you believe in privatization, in other
words, that certain services such as maintenance or
security should be run by the private sector?" Of the
students, 86% (compared with 77% of the delegates)
answered in the affirmative. When asked why they
favored privatization, students (and delegates) cited
the following reasons;

Increased efficiency (38% of students/41 % of
delegates)

Improved services (29% of students/6% of
delegates)

Government inefficiency (17% of students/1 % of
delegates)

Cheaper services (11% of students/21 % of delegates)

These four responses, which all dealt with various
aspects of "efficiency," accounted for 95% of student
responses (versus 63% of delegate responses). The
implication is clear: lopsided majorities of both stu-
dents and delegates agree that the privatization of
selected services in the state's Charity Hospital Sys-
tem could result in enhanced efficiency in one form
or another.

When asked if they thought that contract man-
agement or long-term lease of the Charity System
should be employed, 56% of the students (versus 59%
of the delegates) responded in the affirmative. When
asked why they favored this proposal, 39% of stu-

dents (versus 17% of delegates) again cited "increased
efficiency," and 30% of students (versus 2% of del-
egates) cited "better management." In contrast, 17%
of delegates (versus only 7% of students) had cited
"fipancial considerations," and 15% of delegates (ver-
sus only 7% of students) stated that "The present
system doesn't work well." No other specific reason
was cited by more than 10% of the students or del-
egates responding. Thus, in contrast with the re-
sounding endorsement for "privatization of certain
services," the support for leasing or contract man-
agement of the Charity Hospital System is less clear-
cut. Furthermore, it would appear that students and
delegates who favor these proposals differ in their
reasons for doing so.

Finally, respondents were asked, "What do you
think is the greatest obstacle the Charity Hospital Sys-
tem faces in providing health care?" A total of 37%
of the students (and 35% of the delegates) cited "fi-
nancial considerations." Of students, 13% (but only
6% of delegates) named "civil service" as an "obsta-
cle." Interestingly, only 5% of students mentioned
"politics" as an obstacle, although this factor had been
cited by 30% of the delegates. In any case, a dear
plurality of both students and delegates agree that
financial considerations are a major impediment to
the effectiveness of the Charity Hospital System in
providing health care.

EVALUATION OF CHARITY HOSPITAL
AT NEW ORLEANS

Respondents were asked to rate each hospital, in-
cluding Charity Hospital at New Orleans (CHNO),
on 10 different aspects of medical care, using a nu-
merical scale ranging from "1" (poor) through "3"
(average) to "5" (superior). On eight of the 10 scales,
there was considerable agreement in student and del-
egate assessments of CHNO. Students and delegates
alike rated "Big Charity" above average on "teaching"
and "emergency medical services"; average on "serv-
ice and referral network"; and below average on
"physical plant," "preventive health services," "com-
munications," "rehabilitation services," and "non-
emergency patient care." Mean scores on all of these
items were strikingly similar between students and
delegates.

These areas of agreement are relatively noncon-
troversial and include few surprises. Charity has long

20 JOURNAL VOL 140 AUGUST

i been recognized as an excellent arena for medical ed-
I ucation, and has long set the standard for major trauma
I care in the Greater New Orleans Area. Likewise, it
should come as no surprise that Charity's aging phys-
j ical plant is showing the effects of 50 years of wear
I and tear. I will not dwell any further on these areas
I of basic agreement between students and delegates,
i However, two aspects of medical care at CHNO
I were rated quite differently by students and dele-
j gates. "Perinatal services" were seen as average (3.085)
j by students but below average (2.595) by delegates.

I Five subsidiary questions dealt with various aspects
i of perinatal services, including "medical education,"
"prenatal care," "risk assessment," "inpatient care,"
and "infant transport capabilities." Students consist-
‘ ently rated each of these facets of perinatal services
slightly higher than delegates. Since most delegates
! had been residents or students in the Charity Hospital
System between nine and 12 years prior to completing
the survey, these differences in scores between stu-
^ dents and delegates may well reflect real improve-
j ments in CHNO's perinatal services over the past
^ decade.

On the down side, "nursing support" at CHNO
? was rated below average (1.869) by students, but was
; seen as average (3.398) by delegates. Three subsidiary
questions dealt with different aspects of nursing sup-
i port. "Quality of training" was rated below average
(2.189) by students, but above average (3.558) by del-
egates. "Morale" was rated below average by stu-
dents (1.579) and delegates (2.500) alike. "Profession-
alism" was rated below average (1.643) by students
t but average (3.047) by delegates. Again, in view of
the time lag between students and delegates, these

differences in ratings may reflect real declines in the
quality and professionalism of nursing support at
CHNO in the past decade.

Several essay questions dealt with CHNO in par-
ticular. Respondents were asked "Do you feel that,
from a teaching perspective, CHNO could be re-
placed?" Of students, 80% (versus 54% of delegates)
said "no." Of the 20% of students who felt that CHNO
could be replaced, more than half (52%) suggested
"building a complete new hospital." (Of the delegates
who considered CHNO replaceable, 43% had sug-
gested "utilizing LSU, Tulane, or another teaching
hospital.")

Another essay question stated, "If there are some
strong points and/or weak points of CHNO opera-
tions which you feel are particularly important, please
describe them." "Patient variety and pathology" was
named as a strong point by 44% of students and 35%
of delegates. "Teaching" was considered a strong point
by 19% of students and 35% of delegates. Both 12%
of students and 12% of delegates rated "emergency
care" as a strong point.

Among weak points, "poor treatment/care" was
cited by 34% of students and 22% of delegates. A total
of 26% of students (but only 13% of delegates) named
"understaffed/morale problems" as a weak point. A
total of 15% of delegates (but only 6% of students)
cited the "outmoded facility" as a weak point. No
other single weak point was named by more than 10%
of students or delegates.

Finally, respondents were asked to assign a nu-
merical rank-order to each of 10 possible "alternative
futures" for CHNO. Briefly, the 10 options included
expanding, renovating, restructuring, privatizing.

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leasing, downscaling, or closing CHNO, versus main-
taining the status quo. A total of 57% of students and
52% of delegates regarded the closing or elimination
of CHNO as the least desirable alternative. Maintain-
ing CHNO '"exactly as it is" was the least preferred
alternative for 36% of students and 32% of delegates.

In terms of the desirable outcomes, only 20% of
students (and 28% of delegates) preferred to see
CHNO closed down altogether. Only 2% of students
(and 4% of delegates) preferred to "allow CHNO to
remain exactly as it is." The vast majority (78% of
students and 68% of delegates) wanted to retain
CHNO in some altered form. A total of 25% of stu-
dents and 21% of delegates) preferred to "retain
CHNO but renovate present facilities." Another 25%
of students (and 17% of delegates) recommended to
"retain CHNO but employ . . . contract management
arrangement or long-term lease." A total of 15% of
students (and 7% of delegates) recommended to "re-
tain CHNO . . . and 'contract out' certain key services
to the private sector." Both 5% of students and 5%
of delegates proposed adding beds at CHNO, while
another 5% of students (and 7% of delegates) sug-
gested downscaling CHNO to one-half or one-fourth
of its present size. In summary, a solid majority of
both students and delegates want to see CHNO pre-
served in its present size, but with some combination
of renovation and privatization.

EVALUATION OF

CONFEDERATE MEMORIAL HOSPITAL

Confederate Memorial Hospital in Shreveport was
evaluated by 28 students and 17 delegates. In view
of the small sample sizes, comparisons between the
responses of the two groups must be viewed with
considerable caution. In general, the students rated
Confederate Memorial above average in "emergency
medical services," "physical plant," and "service and
referral network," and average in terms of "perinatal
services," "non-emergency patient care," "teaching,"
"rehabilitation services," "preventive health serv-
ices," and "nursing support."

Neither students nor delegates considered Con-
federate Memorial to be below average on any of the
10 aspects of medical care rated. The delegates rated
"emergency medical services," "teaching," and
"physical plant" above average, while giving Con-

22 JOURNAL VOL 140 AUGUST

federate Memorial average ratings in "communica-
tions," "non-emergency patient care," "preventive
health services," "perinatal services," "service and
referral network," and "rehabilitation services."

Thus, it appears that students and delegates agree
that Confederate Memorial is above average in terms
of its physical plant and its emergency medical serv-
ices and average on six of the other eight scales. The
two areas of minor disagreement between the two
groups are in "teaching," which was more highly
rated by delegates than by students, and "service and
referral network," which was regarded more highly
by students than by delegates. It is perhaps most
noteworthy that Confederate Memorial did not re-
ceive any below average ratings from either group;
this stands in sharp contrast to the results at CHNO.

EVALUATION OF EARL K. LONG
MEMORIAL HOSPITAL

Earl K. Long Memorial Hospital in Baton Rouge was
evaluated by 19 students and 20 delegates. In view
of the small sample sizes, comparisons between the
responses of the two groups must be viewed with
considerable caution. In general, the students rated
Earl K. Long above average in "communications,"
"teaching," "physical plant," and "nursing support,"
and average in terms of "rehabilitation services,"
"service and referral network," "preventive health
services," "non-emergency patient care," and "per-
inatal care." (Students did not rate Earl K. Long on
"emergency medical services.")

The delegates rated "teaching" above average,
while giving Earl K. Long average ratings in each of
the other nine facets of medical care.

Thus, students and delegates agree that Earl K.
Long is above average in terms of teaching and av-
erage on five of the other scales. In each of the three
areas of minor discordance between the two groups
("physical plant," "communications," and "nursing
support"), the students gave higher marks than the
delegates. This may reflect real improvements in each
of these areas over the past decade, in view of the
time lag between students and delegates in terms of
their contact with the system. It is perhaps most note-
worthy that Earl K. Long did not receive any below
average ratings from either group; again, this stands
in sharp contrast to the results at CHNO.

SUMMARY OF SURVEY FINDINGS

• Substantial majorities of both students and dele-
gates see the provision of care to the medically in-
digent as the principal justification for the Louisiana
Charity Hospital System.

• Substantial majorities of both students and dele-
gates endorse the concept of privatization of certain
services in the Charity Hospital System, in the ex-
pectation that this would result in increased effi-
ciency.

• Both students and delegates also support a more
comprehensive concept of privatization involving
leasing or contract management of entire hospitals.
However, the support for this proposal is not as strong
as for selective "contracting out" of key services.

• Financial considerations were seen as the main ob-
stacle faced by the Charity Hospital System, according
to both students and delegates. Students and dele-
gates differed in their perception of political factors
and the Civil Service System as lesser obstacles.

• Charity Hospital of New Orleans (CHNO) was rated
above average in terms of teaching and emergency
medical services by students and delegates alike.

• Students and delegates likewise agreed in ranking
CHNO below average in terms of physical plant, non-
emergency patient care, preventive health services,
communications, and rehabilitation services.

• Students and delegates differed in their ratings of
CHNO on perinatal services and nursing support.
Specifically, students rated perinatal services higher
and nursing support lower than delegates did. These
differences may reflect actual changes in conditions
at CHNO over the past 10 years.

• Substantial majorities of both students and dele-
gates considered CHNO irreplaceable as a teaching
institution.

• Emergency care, patient variety and pathology, and
teaching were cited as CHNO's strong points by stu-
dents and delegates aHke.

• CHNO's weak points, according to students and
delegates, included poor treatment or care, under-
staffing and attendant morale problems, and the out-
moded facility.

• Substantial majorities of both students and dele-
gates would like to see CHNO preserved at approx-

imately the same bed capacity, but with privatization
of at least some services and renovation of the phys-
ical plant.

• Confederate Memorial Hospital in Shreveport re-
ceived higher ratings across the board than did CHNO,
and was considered above average in terms of phys-
ical plant and emergency services by both students
and delegates. No below average ratings were given.

• Earl K. Long Memorial Hospital in Baton Rouge
received even higher ratings than either Confederate
Memorial or CHNO, both from students and dele-
gates. No below average ratings were given, and Earl
K. Long was deemed to be above average in terms of
teaching by students and delegates alike. Addition-
ally, the students gave Earl K. Long above average
ratings for physical plant, nursing support, and com-
munications.

REFERENCES

1. The Charity Hospital System of Louisiana: Physician Views and Evaluations.
New Orleans, Louisiana State Medical Society, Education and Research
Foimdation, December 1986.

Dr Groves is a recent graduate of Louisiana State University School of
Medicine and is presently a resident specializing in internal medicine at
the University of California Davis Medical Center in Sacramento.

Acknowledgments to the LSMS Executive Committee for its support,
foresight, and generosity with these studies of the Charity Hospital
System, and to Dr Eric Hoffman, director of the LSMS Dept of Special
Programs, in tabulating, analyzing, and summarizing the results of

these surveys.

JOURNAL VOL 140 AUGUST 23

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September

September 6-9

3rd Annual Plastic Surgery of the Breast Symposium, San-
ta Fe, New Mexico. Contact: Plastic Surgery Educational Foun-
dation, 444 East Algonquin Rd, Arlington Heights, IL 60005;
(312)228-9900.

September 8-9

How to Select and Evaluate Residents, Boston. Contact: The
American Board of Medical Specialties, PO Box 1280, Evanston,
IL 60204; (312)491-9091.

September 10-18

September 13-16

39th Annual Conference of the American Group Practice
Association: Charting the Course, San Diego. Contact:
AGPA, 1422 Duke St, Alexandria, VA 22314; (703)838-0033.

September 14-19

Cosmetic Surgery of the Face and Breast, Monte Carlo,
Monaco. Contact: Francine Leinhardt, Conference Coordinator,
210 East 64th St, New York, NY 10021; (212)838-9200 ext 2776.

September 17-18

Metropolitan Regional Refresher Course, Las Vegas. Con-
tact: American Society of Anesthesiologists, 515 Busse Hwy, Park
Ridge, IL 60068.

September 17-19

4th Annual Meeting of the American Society for Reconstruc-
tive Microsui^ery, Baltimore. Contact: ASRM, 3025 South
Parker Rd, Suite 65, Aurora, CA 80014.

September 19-30

Autumn Harvest in Sicily: International Symposium on
Acute Care Pediatric Medicine, Rome, Italy and Taormina,
Sicily. Contact: Georgetown University Medical Center, Office of
Continuing Medical Education, 3800 Reservoir Rd NW,
Washington, DC 20007; (202)687-8735.

September 26-29

American College of Emergency Physicians Annual Scien-
tific Assembly, New Orleans. Contact: ACEP, PO Box 619911,
Dallas, TX 75261-9911; (214)550-0911.

September 29-30

Issues and Concerns Facing IRBs and Clincial Investigators,

Austin, Texas. Contact: Office of Continuing Medical Education,
Scott & White, 2401 South 31st St, Temple, TX 76508;
(817)774-2350.

October

October 3-5

October 3-7

6th Annual Comprehensive Review of Vascular Surgery,

Santa Monica, California. Contact: UCLA Extension, PO Box
24901, Los Angeles, CA 90024-0901; (213)825-1901.

October 8-12

American Society of Anesthesiologists Aimual Meeting, San

Francisco. Contact: ASA, 515 Busse Hwy, Park Ridge, IL 60068.

October 8-15

10th International Seminar on Operative Arthroscopy,

Kauai, Hawaii. Contact: UCLA Extension, Dept of Continuing
Education, PO Box 24901, Los Angeles, CA 90024-0901;
(213)825-1901.

October 8-16

13th Annual International Body Imaging Conference, Maui,
Hawaii. Contact: Annual Body Imaging Conference, 21915 Roscoe
Blvd, Suite 222, Canoga Park, CA 91304; (818)700-9821.

October 10-12

7th Annual Cardiology Symposium & Rehabilitation Up-
date, New Orleans. Contact: Patti O'Rourke, RN, Symposium
Coordinator, East Jefferson General Hospital, 4200 Houma Blvd, I
Metairie, LA 70011; (504)454-4145.

October 12-14

Hip and Knee Reconstructive Surgery 1988, Kauai, Hawaii.
Contact: UCLA Extension, Health Sciences Dept, PO Box 24901,
Los Angeles, CA 90024-0901; (213)825-1901.

October 22-23 J

Review Course in Pediatric Orthopaedics, New Orleans.
Contact: Children's Hospital, Dept of Orthopaedics, 200 Henry
Clay Ave, New Orleans, LA 70118; (504)891-7067.

26 JOURNAL VOL 140 AUGUST

October 26-30

AMA 9th National Conference on Impaired Health Profes-
sionals: Visions and Values, Chicago. Contact: AMA, 535
North Dearborn St, Chicago, IL 60610; (800)621-8335.

November

November 2-5

Optimizing Management of Primary Bone Tumors: An In-
ternational Symposium Emphasizing the Multidisciplinary
Approach, Houston. Contact: Office of Conference Services,
M.D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston,
TX 77030; (713)792-2222.

November 2-5

The Wrist 1988, Saddlebrook Resort, Tampa, Florida. Con-
tact: American Society for Surgery of the Hand, 3025 S Parker Rd,
Suite 65, Aurora CO 80014; (303)755-4588.

November 5

November 10-13

Lasers for the Plastic Surgeon, Orlando, Florida. Contact:
Plastic Surgery Educational Foundation, 444 East Algonquin Rd,
Arlington, Heights, IL 60005; (312)228-9900.

November 11-12

November 17-20

Assuring the Future Fiscal Siuvival of Consultation —
Liaison Psychiatry and Psychosomatic Medicine, New

Orleans. Contact: Academy of Psychosomatic Medicine, 5824 N
Magnolia, Chicago, IL 60660; (312)784-2025.

November 19-20

American Society of Anesthesiologists Workshop on
Obstetrics, Kansas City, Missouri. Contact: ASA, 515 Busse
Hwy, Park Ridge, IL 60068.

November 27 - December 2

74th Scientific Assembly and Annual Meeting of the

Radiological Society of North America, Chicago. Contact:
RSNA, 1415 W 22nd St, Tower B, Oak Brook, IL 60521;
(312)571-2670.

December

December 2-4

Ninth Annual Perinatal Postgraduate Course, Jackson,
Mississippi. Sponsored by the University of Mississippi
School of Medicine. Contact: University of Mississippi Medical
Center, 2500 North State St, Jackson, MS 39216-4505;
(601)984-1300.

December 3-6

Workshop in Reconstructive Surgery of the Hand, New

York. Sponsored by the American Society for Surgery of the
Hand. Contact: Terri Harrington, American Society for Surgery
of the Hand, 3025 South Parker Rd, Suite 65, Aurora, CO 80014;
(303)755-4588.

December 4-5

Child Development Course, New Orleans. Sponsored by
Alton Ochsner Medical Foundation. Contact: Ochsner Office
of Continuing Medical Education and Alumni Affairs, 1516 Jef-
ferson Hwy, New Orleans, LA 70121; (504)838-3702.

December 4-5

Contemporary Concepts in Facial Surgery, The Waldorf
Astoria Hotel, New York. Sponsored by Manhattan Eye, Ear
and Throat Hospital in conjunction with The Institute of
Reconstructive Plastic Surgery of the New York University
Medical Center. Contact: Francine Leinhardt, Course Coordinator,
Manhattan Eye, Ear and Throat Hospital, 210 East 64th Street,
New York, NY 10021; (212)838-9200 ext 2776.

December 4-6

Reconstructive Surgery of the Hand, Valhalla, New York.
Sponsored by American Society for Surgery of the Hand.
Contact: American Society for Surgery of the Hand, 3025 South
Parker Rd, Suite 65, Aurora, CO 80014; (303)755-4588.

December 5-12

Post-RSNA Imaging at Sea Caribbean Cruise, Contact:
Medical Seminars International Inc, 21915 Roscoe Blvd, Suite 222,
Canoga Park, CA 91304; (818)340-0580 ext 280.

December 7-9

American Cancer Society National Conference on Advances
in Cancer Management, Los Angeles. Contact: American
Cancer Society, 90 Park Ave, New York, NY 10016; (212)599-3600.

JOURNAL VOL 140 AUGUST 27

THE COCAINE EPIDEMIC:

DRUG ABUSE PATTERNS IN NEW ORLEANS

BARRY D. SCHWARTZ, PhD; LARRY MURRAY;
BETTY ALEXANDER, MSW; FRANK R. KAUDERS, MD;

DON GALLANT, MD

28 JOURNAL VOL 140 AUGUST

This present study was undertaken to evaluate the
changing patterns of drug abuse in New Orleans.
All of the patients admitted to the New Orleans
Veterans Administration Hospital Drug
Rehabilitation Unit in 1975 (175 subjects), 1980 (204
patients), and in 1985 (215 patients) were evaluated
for their preference of drugs of abuse as well as to
possible significant differences in age, marital
status, race, and education. At the same time,
another drug incidence survey was conducted at a
private university in New Orleans to determine
whether there was a significant difference in drug
trends between the college students and the
veterans admitted to the Drug Rehabilitation Unit.

Comparison of the New Orleans Veterans
Administration Hospital data with the drug
incidence data on the college campus and a High
School Senior Survey conducted by the University
of Michigan indicated that cocaine will be the drug
of choice for the next several years. All drug
detoxification and rehabilitation programs should
now be in the process of revising the treatment
approaches to incorporate new specific treatment
modalities for this widely abused drug.

G eogbiaphic accessibility, as well as cultural and
psychological attitudes, play an important role
in the acceptance or rejection of drugs that have the
potential for abuse. ^ Two other important factors that
affect the pattern of substance abuse are peer impact
and legal approaches to the problem. In view of the
recent reported nationwide increase in the use of co-
caine, the present study was undertaken to determine
whether or not such an increase was occurring in New
Orleans, a port city which is relatively close to the
major areas of cocaine origin.

A prior investigation of drug use patterns in 1975
and 1980 of aU patients admitted to the New Orleans
Veterans Adrninistration Medical Center (NOV AH)
Drug Dependence Treatment Program (DDTP) indi-
cated that heroin was the most frequently cited drug
of choice both in 1975 and 1980, although it was start-
ing to show a downward trend in 1980.^ “T's & Blues"
(Talwin and pyrabenzamine) increased independ-
ently and in association with certain demographics.
A trend toward lower preferences for marijuana and
"downers" (tranquilizers and hypnotics) as drugs of
first choice was observed in 1980 as compared to 1975,
while stimulant use, Preludin and cocaine, was show-

ing an increase in 1980.

In the current study, descriptions of drug abuse
patterns were obtained from all patients admitted to
the NOVAH-DDTP in 1980 (204 patients) and 1985
(215 patients). This drug treatment unit is the only
government drug rehabilitation unit in New Orleans
and is the oldest established drug rehabilitation ward
in the area. The great majority of the patients admitted
to the unit come from lower and middle income classes.
These patients were evaluated as to their preference
of drugs in order of first and second choice. Addi-
tionally, sociodemographic variables of age, race,
method of support, marital status, and educational
level were recorded.

RESULTS

Table 1 presents the frequency and percentage dis-
tribution of selected sociodemographic variables and
their respective chi-square values. The proportion of
blacks, whites, and others did not significantly differ
between 1980 and 1985; significantly fewer patients
were married in 1985, while the proportion in the
single and other categories remained approximately
the same. As compared to 1980, fewer patients had
less than a high school education in 1985. The means
of support by patients in 1985 had shifted from illegal
or work only to work and/or illegal methods of sup-
port.

There were approximately 20 drugs listed as first
and second drugs of choice (if the first drug were
unavailable) by the patients. Half of the choices listed
appeared so infrequently that they were not incor-
porated into the final chi-square analysis. Table 2
shows the drugs of abuse most frequently cited, their
frequency of use, and the percentage of patients
choosing that drug for each of the two years. The
table indicates the profile of first choice drugs of abuse
significantly shifted from heroin and "T's & Blues"
in 1980 to cocaine, heroin, and marijuana in 1985. A
similar reversal in the second choice drugs of abuse
occmred. The 1980 second choices were primarily Pre-
ludin and "T's & Blues," while in 1985, cocaine, her-
oin, and marijuana maintained their selection status.

It is interesting to note that race was not asso-
ciated with drug abuse (p > .05) nor was marital status
(p > .05). The noted drug choice profiles for 1980 and
1985 were constant for age and education. Thus, all
ages and education levels showed a significant switch ^

JOURNAL VOL 140 AUGUST 29

TABLE 1

NEW ORLEANS VETERANS ADMINISTRATION HOSPITAL-DRUG DEPENDENCE TREATMENT PROGRAM PATIENTS

Number of Patients
1980 %

Number of Patients
1985 %

Age

19-24

5.9

5.8

25-29

120

39.0

21 .9*

30-34

27.3

33.0

35-39

11.1

30.7*

40 & above

16.6

8.8*

^2 - 44.2, df - 4, p < 0.05

Race

Black

221

73.0

139

65.0

White

27.0

35.0

= 3.69, df = 1 , p > .05
Marital Status
Married

104

33.8

27.6*

Single

129

41.9

36.9

Others

24.4

35.5

X" = 7.77, df = 2, p < 0.05
Education
< High School

27.9

12.1*

= High School

146

47.9

105

48.8

> High School

24.7

39.1

^2 = 23.44, df - 2, p < 0.05

Method of Support

Illegal

103

33.4

11.2*

Work

30.5

34.0

Both

111

36.0

108

54.8*

X^ = 34.32, df = 2, p < 0.05

* indicate p < .05 (1980 vs. 1985)

in choice from heroin, “T's & Blues," and Preludin
as first and second choices in 1980 to cocaine, heroin,
and marijuana as first and second choices in 1985.

DISCUSSION

In our previous study of drug use by the patients
admitted to this drug rehabilitation unit during the
years 1975 and 1980, there was an indication that use
of stimulant drugs was increasing, in association with
a relative decrease in sedative drug use.^ However,
heroin was the preferred drug of choice in 1975 and
1980. The present data indicate that, in contrast to
1975 and 1980, cocaine has now been elevated to the
status of the most frequently preferred first drug
(50.5%) and second drug (23.1%). It is interesting to

30 JOURNAL VOL 140 AUGUST

note that the 1975-80 study indicated that cocaine use
was restricted primarily to white, single individuals,
while the present study shows that race is not asso-
ciated with drug choice (p > 0.05). Thus, we see the
increase in cocaine use moving across the demo-
graphic boundaries of race, marital status, age, and
education levels.

In another ongoing series of drug incidence sur-
veys conducted at a private university in New Orle-
ans, the greatest difference in drug use between 1972
and 1986 was a 16-fold increase in those students who
used cocaine more than 10 times (Table 3).

Heroin has relinquished its status of first drug of
choice. Thus, the profile for the drug abuser of 1985
compared to 1980, as seen in the NOVAH-DDTP, is

TABLE 2

FREQUENCY AND PERCENTAGES OF FIRST AND SECOND CHOICE DRUGS 1980-1985

Drug

First Choice

Second Choice

1980

1985

1980

1985

ETOH

3.1

6.5

5.1

12.6

Amphetamines

2.4

2.7

5.8

2.7

Cocaine

5.5

50.5*

9.7

23.1*

Dilaudin

3.1

1.6

40.4

3.8*

Heroin

138

47.1

15.2*

6.1

13.2*

Marijuana

3.1

19.0*

10.5

33.5*

Preludin

6.5

1.1

23.5

0.5*

T’s & Blues

23.2

.5*

18.1

5.5*

Valium

6.1

2.7

6.9

4.9

= 219.1 1, df = 8, p < 0.01 First Choice
= 124.9, df = 8, p < 0.01 Second Choice
*p < .05 (1980 vs. 1985)

an individual who is most likely to be older (30-39
j years of age versus 25-39), is as likely to be married
as unmarried, has a greater likelihood of having a
minimum of a high school education, supports his
addiction by work and/or illegal methods, and selects
cocaine and marijuana as his primary drugs of choice.
Comparing these data with the drug incidence data
on the college campus and a High School Senior Sur-
vey conducted by the University of Michigan, it ap-
pears that cocaine will be the drug of choice for the
next several years. ^ All drug detoxification and re-
habilitation programs should now be in the process
of revising the treatment approaches to incorporate
new specific treatment modalities for this widely
abused drug. ■

REFERENCES

1. Gallant DM: Alcoholism: A Guide to Diagnosis, Intervention, and Treatment.
New York, WW Norton & Co Inc, 1977, pp 35-46.

2. Kandel D: Stages in adolescent involvement in drug use. Science
1975;190:912-914.

, 3. Smart RG: The New Drinkers. Ontario, Canada, Addiction Research Foim-

; dation, 1971.

! 4. Schwartz BD, Murray L, Alexander B, et al: / La State Med Soc 1982;134:48-

( 50.

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